Care of the Patient with Hepatobiliary Tract Disorders PDF

The liver, gallbladder, and exocrine pancreas are organs that assist with digestion. 1. Learning Step / Activity 1. **Cirrhosis**. a. Etiology/Pathophysiology: 1. Chronic, degenerative disorder of the liver f rom generalized cellular damage. a. Lobes are covered with f ib...

The liver, gallbladder, and exocrine pancreas are organs that assist with digestion. 1. Learning Step / Activity 1. **Cirrhosis**. a. Etiology/Pathophysiology: 1. Chronic, degenerative disorder of the liver f rom generalized cellular damage. a. Lobes are covered with f ibrous tissue. b. Liver parenchyma (tissue) degenerates. c. Lobules (functional unit of liver) are inf iltrated with fat. d. Fibrous tissue restricts blood f low, leading to further destruction. e. Hepatomegaly, then progressively later, liver contraction (shrinkage) occurs. 2. The liver becomes increasingly unable to carry out its many functions. Consequently, there are: f. Disturbances in digestion and metabolism. 1. Inability to convert ammonia to urea, resulting in elevated serum ammonia levels. 2. Reduced protein synthesis (albumin) with decreased plasma oncotic (colloidal) pressure, resulting in third spacing f luids. g. Defects in blood coagulation. h. Defects in fluid and electrolyte balance. 3. Ascites: accumulation of third spaced fluid and albumin in the abdomen (due to portal hypertension, hypoalbuminemia and elevated levels of aldosterone). 4. Low circulating volume signals the release of aldosterone. i. Impairments in ability to metabolize hormones and detoxify chemicals. j. Portal hypertension, esophageal varices, ascites and hepatic encephalopathy. 3. Cirrhosis develops slowly over many years. k. With repeated insults, the liver progresses through stages: 5. Destruction. 6. Inf lammation. 7. Fibrotic regeneration. 8. Hepatic insufficiency. l. Liver cells have great potential for regeneration, but repeated scarring decreases their ability to be replaced. m. The cause is not always known; however, alcohol is by far the greatest factor leading to cirrhosis. 4. Major types of cirrhosis: n. Alcohol-related liver disease: 9. May occur with heavy alcohol consumption. 10. Affects more men than women. 11. The amount of alcohol that causes liver damage differs among individuals. 12. Chances increase for men and women when alcohol consumption is greater than 3-4 drinks per day. 13. Most common type of cirrhosis. o. Post-necrotic cirrhosis: 14. Found worldwide. 15. Caused by viral hepatitis, exposure to hepatotoxins or infection. p. Biliary or obstructive cirrhosis: 16. Primary: a. Results f rom chronic obstruction or inf lammation of the bile ducts. b. Found more often in women. 17. Secondary: c. Caused by chronic biliary tree obstruction by gallstones, tumor or biliary atresia in children. 18. Cardiac cirrhosis: d. Associated with severe right sided CHF with *cor pulmonale,* 19. Nonalcoholic fatty liver disease (NAFLD): e. Results f rom fat build up in the liver. f. Incidence is on the increase due to growing obesity population. 1. Symptoms occur when severe liver damage is present: a. Headache b. Anorexia b. Nausea and vomiting c. Indigestion d. Diarrhea or constipation e. Palpable liver (f ) Abdominal pain g. Dyspepsia (indigestion) h. Changes in bowel habits. 2. Tissue wasting with fatigue and weakness. 3. Weight loss that may be masked by f luid retention. 4. Ascites (accumulation of f luid and albumin in the peritoneal cavity) and peripheral edema: c. Marked abdominal distention. d. Edema of lower extremities. e. Decreased formation of plasma albumin (hypoalbuminemia) contributes to ascites and edema. f. Dyspnea results f rom intra-abdominal pressure on diaphragm. g. Dilated veins over the abdomen (caput medusae) due to portal hypertension. 5. Other Manifestations of Portal Hypertension: h. Splenomegaly. i. Prominent, distended abdominal blood vessels. j. Distended blood vessels in esophagus, stomach (varices) and rectum (hemorrhoids). Video link (Portal Hypertension) -------------------------------- 6. Bleeding Tendencies: k. Result of varices and hemorrhoids, impaired formation of clotting factors, and impaired absorption of Vitamin K. l. May include: 1. Bleeding f rom GI tract (hematemesis, blood in stools). 2. Easy bruising m. Anemia 7. Jaundice (Icterus): n. Yellowish discoloration of tissues caused by abnormally high level of bilirubin in blood. o. Liver is unable to transform the bilirubin into its conjugated (direct) form and secrete it into the bile ducts. p. Jaundice becomes visible when serum bilirubin levels reach 2.5 mg/dl or higher. q. Stools become clay-colored. r. Urine becomes deep orange in color. 8. Skin Changes: s. spider telangiectases (small, dilated blood vessels with a bright red center point and spider-like branches). t. Palmar erythema u. Pruritus v. Loss of body hair 9. Decreased renal function c. Assessment: 1. Subjective: a. Early stages: 1. Nausea, vomiting 2. Loss of appetite 3. General weakness, fatigue 4. Indigestion, f latulence, constipation/diarrhea, abdominal discomfort. b. Later stages: 5. Above symptoms, but more intense 6. Dyspnea 7. Severe fatigue with inability to complete ADLs. 2. Objective: c. Early stages: 8. Anemia 9. Fever 10. Jaundice 11. Weight loss d. Later stages: 12. Epistaxis, purpura, hematuria, spider hemangiomas, bleeding gums 13. Ascites 14. Coagulopathy, hemorrhage (f rom esophageal varices or other distended veins) 15. Splenomegaly 16. Disorientation, abnormal behavior and speech patterns d. Diagnostic Findings: 3. Elevation of liver enzymes: e. ALT (alanine aminotransferase) f. AST (aspartate aminotransferase) g. LDH (lactic dehydrogenase) h. Gamma GT 4. Decreased serum albumin, elevated ammonia and decreased glucose. 5. Abnormal CBC 6. Prolonged PT 7. Abnormal urinalysis 8. Visualization: i. ERCP (for common bile duct obstruction) j. Esophagoscopy with barium esophagography (for varices) k. Scans and biopsy of the liver l. Ultrasound 9. Paracentesis: laboratory examination of ascites f luid. (Fluid is drawn f rom the peritoneum for lab analysis and to relieve ascites with dyspnea.) e. Medical Management: Eliminating (e.g., **acetaminophen, Tylenol)** 10. Eliminate causes 11. Decrease buildup of fluids m. Initiate bedrest 17. Indicated when liver is deteriorating, during fever or infection 18. Head of bed elevated to facilitate breathing n. Sodium and fluid restriction. (Diet restriction: 500-1000 ml fluid and 1000 mg to 2000 mg sodium). o. Daily weight p. Strict I&O d. Diuretic therapy 1. Spironolactone: 300 to 1000mg/day. (Aldactone antagonist increasing Na+ and Cl- wasting, while sparing K+.) 2. Lasix 3. Hydrodiuril (hydrochlorothiazide) e. Salt-poor albumin infusions to restore plasma volume. f. LeVeen shunt (see below) g. Paracentesis (see below) h. Measure abdominal girth daily and check ankles for edema. Video link to Diuretics overview: --------------------------------- 12. Prevent further damage to liver: q. Eliminate alcohol, hepatotoxins or environmental exposure to harmful chemicals. r. Monitor closely for drug toxicity as liver function decreases (especially medications cleared by the liver). 13. Provide individual supportive care to patient. s. Provide diet high in calories and carbohydrates with adequate protein supplemented with vitamins and minerals. (Vitamin supplements K, C and folic acid given.) t. Low-fat and low-sodium is indicated. u. Protein intake is restricted in clients with advanced liver disease because it increases the amount of ammonia in the intestine, precipitating hepatic encephalopathy. v. Frequent, small, easily digested meals may be better tolerated. w. Anti-emetics to control nausea and vomiting. x. Manage esophageal varices (see below). 14. Paracentesis procedure: y. Ascitic fluid is removed from the peritoneal cavity by gravity or vacuum. z. Performed for diagnostic purposes and when patient has severe abdominal distention and respiratory distress. a. Performed very cautiously as severe complications could result. 19. Hypovolemic shock from sudden shift of fluid from circulatory system to the peritoneum to replace aspirated fluid. 20. Perforation of abdominal organs (to include bladder). 21. Wound infection. b. Patient must void immediately before the procedure to prevent bladder puncture. 22. Position patient at side of bed in high Fowlers. Incision is made and a hollow trocar, (cannula or catheter) is passed through the incision. 23. Fluid removed over 30 to 90 minutes to prevent changes in B/P. 24. Monitor patient for hypovolemia and electrolyte imbalance. Monitor dressing for bleeding and drainage. 15. Peritoneal Jugular Shunt (LeVeen shunt): c. Catheter is placed by physician to shunt ascitic f luid f rom peritoneal cavity. d. A one-way valve allows movement of ascitic f luid f rom the peritoneal cavity to the superior vena cava when the peritoneal cavity pressure increases. e. Complications: 25. Hemodilution. 26. Pulmonary edema, congestive heart failure. 27. Wound infection, peritonitis, septicemia (bacteria in the blood). 28. Occlusion of the shunt by thrombus. 16. Monitor for and prevent bleeding: f. Assess stools, emesis, gums, skin for bleeding. g. Vitamin K, FFP (f resh f rozen plasma) infusions to replace clotting factors. Important, particularly before invasive procedures, i.e., paracentesis. 17. Monitor and prevent complications: h. Portal hypertension and esophageal varices - Varices can rupture as a result of anything that increases abdominal venous pressure, such as coughing, sneezing, vomiting, or the Valsalva maneuver. Remember patient teaching to avoid coughing, just like with painful pancreatits! 29. Intrahepatic veins in the scarred cirrhotic liver meet resistance, resulting in blood backing up into the portal vein and into diverting channels in the esophagus and stomach. 30. Veins in esophagus become dilated and tortuous (varices) and may bleed. 31. Can rupture over several days or suddenly. Patients present with bright red hematemesis (vomiting blood). Patients can experience significant blood loss during variceal bleeds. 32. Management of a ruptured esophageal varix is a medical emergency requiring the following: a. Airway (may be an issue with massive hematemesis/aspiration). b. Insert IV lines (2 large bore- at least 18-gauge for blood transfusion). c. Vasopressin, (potent vasoconstrictor) IV directly into vena cava, to decrease hemorrhage. VP produces vasoconstriction of the vessels, decreases portal blood f low, and decreases portal hypertension. Current drug therapy in some institutions includes a combination of VP and nitroglycerin (NTG). NTG reduces the detrimental effects of VP, which include decreased coronary blood f low. d. Gastric lavage with iced isotonic saline solution. (Removes blood f rom the stomach. Ice water may assist with vasoconstriction to control bleeding.) e. Endoscopic sclerotherapy. (Vasopressin or similar medication is injected into bleeding varices to cause vasoconstriction.) f. Sengstaken-Blakemore tube (see p. 1454): 1. The tube is passed through the nose and into the stomach. Contains two balloons one for the esophagus and the other rest at the end of the tube in the stomach. One or both balloons are inf lated to control bleeding. 2. Controls bleeding varices by inf lating to press against gastric and esophageal vessels. 3. A Levin tube is passed into the esophagus through the mouth and attached to low suction to drain the saliva that cannot drain into the stomach 4. The esophageal balloon must deflated periodically to prevent necrosis 18. Surgical Shunting Procedures: i. Goal is to shunt blood around the liver to decrease potential backup and esophageal bleed. j. These procedures have a high mortality. k. Complications are worsening hepatic encephalopathy, GI bleeding, ascites and liver failure. l. Types of Shunts: 33. Portacaval shunt: blood is diverted f rom the portal vein to the inferior vena cava. 34. Splenorenal shunt: removal of the spleen with the splenic vein attached to the lef t renal artery. 35. Mesocaval shunt: anastomosis of the superior mesenteric vein to the inferior vena cava. 19. Supportive Care of patient with Ruptured Varices: m. Maintain O2 content. n. Blood transfusions with whole blood to supply clotting factors. o. Electrolyte replacements. p. Use of cathartics (lactulose) to remove ammonia and enemas to remove blood in intestinal tract. q. Antibiotics to destroy colonic bacteria. 20. Hepatic encephalopathy: central nervous system (CNS) manifestation of liver failure that often leads to coma and death. Consequent ammonia intoxication. It is thought to result f rom a damaged liver being unable to metabolize substances that can be toxic to the brain, such as ammonia. (Ammonia levels will be elevated)!!! r. Ammonia formed in the intestine by bacterial action on proteins is normally detoxified in the liver by conversion to urea. s. A failing liver is unable to break down ammonia and allows it to accumulate in the blood. t. Ammonia can cross the blood-brain barrier and enter brain cells where it interferes with brain metabolism, cell membrane pump mechanisms and neurotransmission. u. Signs and symptoms progress f rom inappropriate behavior, disorientation, f lapping tremors and twitching extremities to stupor and coma. v. The increased ammonia level is related to the development of hepatic coma. w. Therapy to reduce blood ammonia level improves the comatose state. 36. Reduction of protein intake (low protein to no protein diet. (Must maintain adequate caloric intake using carbohydrates). 37. Removal of residual protein or blood f rom the intestines by laxatives and enemas (Lactulose). g. Serum ammonia concentration is also decreased by administering lactulose. Goal of medication is **Improved mental status.** h. In the colon, lactulose splits into lactic acid and acetic acid, attracts the ammonia f rom the blood and forms a compound that can be eliminated in the feces. i. Given orally or as a retention enema or via NG tube. f. Nursing Interventions: 21. Vital signs Q4 hours: x. Report abnormal values. y. Monitor for hemorrhage. b. Instruct patient to avoid straining at stool, vigorous nose blowing and to use a soft toothbrush. c. Administer IM medications, if necessary, with small gauge needles, apply longer gentle pressure after injection. 22. Monitor f luid and electrolyte status: z. Strict I&O a. Monitor labs and report abnormal values. b. Daily weight c. Assess peripheral edema, abdominal girth daily. 23. Provide appropriate, adequate nutrition: d. Low-protein, low sodium, high carbohydrate diet. e. Fluid restriction as ordered. f. Medicate with anti-emetics, as ordered for nausea, vomiting. 24. Provide meticulous skin care: g. Turn patient at least every two hours. h. Use foam or f lotation mattress. i. Use minimal or no soap for bathing; apply lotion to skin to avoid puritis. 25. Monitor mental status and report changes: avoid or use cautiously drugs detoxified by the liver such as Acetaminophen, barbiturates and narcotics. 26. Teach/assess understanding of avoiding contributing factors (i.e., alcohol): j. Provide understanding and non-threatening environment to discuss lif estyle modifications. k. Encourage patients to participate in community activities/support groups. 27. Prognosis: related to the cause of the disease, the susceptibility of the individual and the extent of the involvement: +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. 5. | +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. | +-----------------------------------+-----------------------------------+ 2. Learning Step / Activity 2. **Hepatitis**. \*Review 46.1 on page 1458 and safety alert on page 1459. --------------------------------------------------------- b. Etiology/Pathophysiology: 5. Inf lammation of the liver resulting f rom several types of viral agents, exposure to toxic substances or lengthy alcohol abuse. 6. Acute or chronic. 7. The most common cause of hepatitis is a viral infection: q. The viruses that infect the liver are identified by letters (A, B, C, D, E, F and G). r. They are distinguished by their mode of transmission and incubation period. 8. Hepatitis A (formerly infectious hepatitis): s. Most common. t. Short incubation period of 10 to 40 days. u. Mode of Transmission: by direct contact via the fecal oral route, usually by food or water contamination with feces. 9. Hepatitis B (formerly serum hepatitis): v. Long incubation period: 28 to 160 days. w. Mode of Transmission: contact with contaminated blood and body f luids. 20. Blood 21. Semen and vaginal secretions 22. Saliva 23. Breast milk 24. Needles, syringes, surgical or dental equipment 10. Hepatitis C: x. Incubation Period 2 weeks to 6 months (commonly 6 to 9 weeks). y. Transmitted through needle sticks, blood transfusions. 11. Hepatitis D (also called Delta virus): z. Incubation period 2-10 weeks. a. Mode of Transmission: contact with contaminated blood and body f luids (see above). b. May progress to cirrhosis and chronic hepatitis. [[https://www.osmosis.org/learn/Hepatitis\_B\_and\_Hepatitis\_D\_virus]](https://www.osmosis.org/learn/Hepatitis_B_and_Hepatitis_D_virus) 12. Hepatitis E (formally called enteric non-A-non-B): c. Transmitted through fecal contamination of water- usually in developing countries with poor sanitation and water quality. d. Incubation periods 15 to 64 days. 13. Hepatitis F and G (newest): e. Has been found in blood donors and can be transmitted by transfusion. f. Transmitted through water and food contamination. 14. The pathological f indings in all seven forms of viral hepatitis are identical. g. Diffuse inf lammatory reaction, resulting in liver cells degenerating and dying. h. As the liver cells degenerate, the normal functions of the liver slow down. 15. Health officials are required, by law, to report all cases of viral hepatitis to the Centers for Disease Control and Prevention (CDC). c. Clinical Manifestations: 16. Symptoms vary greatly. 17. Some patients are asymptomatic, whereas others develop hepatic failure or hepatic encephalopathy. d. Assessment: 18. Subjective: i. General malaise, arthralgia (aching joints) lasting for several weeks and weakness. j. Headaches and chills. k. Photophobia. l. Right upper quadrant discomfort, nausea, diarrhea and constipation. m. Pruritus. 19. Objective: n. Jaundice f rom body\'s inability to metabolize bilirubin (yellow skin, discoloration of the sclera and mucous membranes). o. Pruritus f rom the presence of bile on the skin. p. Dark, amber urine. q. Clay-colored stools. r. Hepatomegaly with lymphadenopathy. s. Weight loss and rhinitis. e. Diagnosis: 20. Elevated direct bilirubin, gamma GT, AST, ALT, LDH and alkaline Phosphatase. 21. Prolonged prothrombin time. 22. Leukopenia and hypoglycemia may be present. 23. Serum is examined for presence of HAA (Hepatitis Associated Antigen A, B, C, D, G). 24. No test is available for Hepatitis E. f. Medical Management: 25. No specific treatment other than supportive therapy for signs and symptoms. 26. Prevention of transmission. 4. Bedrest for several weeks is usually recommended. 5. No alcohol for 1 year: may need community assistive services for compliance. 6. Avoid sedative medications. 7. Low-fat, high-carbohydrate diet with vitamin supplements (C, B and K). a. Vitamin C for healing. b. Vitamin B complex to assist in the absorption of fat-soluble vitamins. c. Vitamin K to combat prolonged coagulation time. g. Methods Used to Prevent the Diseases: 27. Hepatitis A: t. Gamma globulin or immune serum globulin given as soon as possible to persons who have been in direct contact with a person with Hepatitis A during the infectious period (2 weeks before and 1 week after onset of symptoms). u. Vaccine for Hepatitis A is recommended: if traveling to developing countries, healthcare workers, homosexual and bi-sexual men, patients with chronic hepatitis and IV drug users. v. Primary immunization with Hepatitis A vaccine (Havrix, Vaqta and Avaxim). 2. Contraindications: a. Hypersensitivity to alum b. Hypersensitivity to 2-phenoxyethanol c. Acute febrile illness (pediatrics) 3. Adverse reactions/side effects d. Local soreness e. Headache 28. Hepatitis B: w. After exposure to Hepatitis B after a needle stick administer Hepatitis B immune globulin (HBIG) with dose repeated 1 month later. x. All health care workers, persons with high-risk lif estyles (as identified above) and infants born to mothers with positive Hepatitis B antigen titers in high-risk areas should be vaccinated for protection. y. Primary immunization with Hepatitis B vaccine (Engerix-B, Recombivax HB) 25. Dosage and Route: g. 3 doses of 1 ml IM, given at 0, 1 -- 2 and 4 -- 6 months. 26. Contraindications: b. Anaphylactic allergy to yeast 27. Adverse reactions/side effects c. Local soreness 29. Good sanitation and personal hygiene. 30. Effective sterilization procedures. 31. Careful screening of food handlers and blood products. h. Nursing interventions: 32. Ensuring rest. 33. Maintain adequate nutrition. 34. Provide adequate f luids. 35. Care for the skin. 36. Prevent further transmission: z. Implement universal precautions. Stress importance of good handwashing and hygiene. a. Teach/assess understanding of modes of transmission and means of prevention. 37. Teach/assess understanding of the signs/symptoms of hepatitis (relapses are common). b. Clay-colored stools. c. Dark, amber colored urine. d. Jaundice. e. Fever. f. GI disturbances. g. Bleeding tendencies. 38. Patient Education: h. Avoid alcohol and giving blood. +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. | +-----------------------------------+-----------------------------------+ | | 1. Provide high carb, low fat | | | diet f luid intake of 2500 to | | | 3000 ml daily | | | | | | 2. 3. 4. Note color and | | | consistency of stool and | | | color and amount of urine. | | | | | | 5. 6. 7. | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. | +===================================+===================================+ | | 1. 2. 3. 4. 5. | +-----------------------------------+-----------------------------------+ a. Etiology and Pathophysiology - primary tumors - cholangiomas - biliary duct carcinomas. b. Risk Factors - Cirrhosis of the liver and infection with hepatitis C or hepatitis B (high-risk) factors for primary liver cancer. - The increase in cases of primary liver cancer stems f rom the increased incidence of hepatitis B. - Increasing age, obesity, type 2 diabetes, male gender, cirrhosis, and hepatotoxins are some of the risk factors tied to liver cancer. - Metastatic carcinoma of the liver, or secondary liver cancer, occurs more often than primary liver cancer. - The high rate of blood f low through the portal vein and its massive capillary structure make the metastasis of cancer cells to the liver more likely than to other organs. The pancreas, colon, stomach, breast, and lung are common primary sites of cancer that metastasizes to the liver. c. Clinical Manifestations - Dull abdominal pain in the epigastric or right upper quadrant region - jaundice, anorexia, nausea and vomiting. - extreme weakness - Palpation may reveal an enlarged, nodular liver. - May experience a pulmonary emboli. d. Diagnostic Tests - liver scan, ultrasound - CT scan, or MRI magnetic resonance imaging, - hepatic arteriography, ERCP, and needle liver biopsy. - Serum liver function tests can be an early indication that the liver is not functioning properly, but this is not always a routine lab test. - alpha-fetoprotein (AFP) may be positive in hepatocellular carcinoma. AFP helps distinguish primary cancer f rom metastatic cancer. e. Medical Management - Treatment of cancer of the liver is largely palliative. - Surgical excision (lobectomy) sometimes is performed if the tumor is localized to one portion of the liver. - Only a small percentage of patients have surgically resectable disease; usually the cancer is too advanced for surgery when it is detected. - Surgical excision or transplantation offers the only chance for cure. Medical management is similar to that for cirrhosis of the liver. - Chemotherapy may be used, but the response is usually poor. Portal vein or hepatic artery perfusion with chemotherapy agents such as 5-fluorouracil (5-FU) may be attempted. f. Nursing interventions for the patient with liver carcinoma and prognosis - Main focus is keeping the patient as comfortable as possible. - This is because the problems are the same as with advanced liver disease, the nursing interventions discussed for cirrhosis of the liver apply. - Prognosis is a 5-year survival rate for liver cancer - although this depends on the extent of the cancer when it is diagnosed. - Localized liver cancer (cancer has not spread past the liver) 5-year survival rate is approximately 31%. - Regional stage liver cancer (involves the liver and nearby lymph nodes and organs) 5-year survival rate is 11%. - Unfortunately, the 5-year survival rate for distant liver cancer (metastases to distant organs or tissues) is 3%. If liver cancer is detected early and the patient has a liver transplant, the 5-year survival rate is 60% to 70% 3. Learning Step / Activity 4. **Liver Abscesses**. Method of Instruction: Lecture i. If an infection develops anywhere along the GI tract, there is a change of infecting organisms reaching the liver through the biliary system, portal venous system, or hepatic arterial or lymphatic systems, and creating an abscess (a collection of pus). 39. Etiology/Pathophysiology i. Bacterial toxins attack neighboring liver cells and necrotic tissue produced is protective wall for the organism. j. Leukocytes migrate into the infected area: i. Result is an abscess. ii. Pyogenic abscesses of this type may be single or multiple. k. Common sources of liver abscesses i. Abdominal infections such as, 1. Appendicitis 2. Diverticulitis 3. Perforated colon ii. Other causes, any infection in: 4. The blood 5. The bile ducts 6. Trauma to the liver 40. Clinical Manifestations l. Vague signs and symptoms m. Fever, with chills n. Abdominal pain and tenderness to right upper quadrant o. Unintentional weight loss p. Jaundice (f ) Weakness 41. Assessment q. Subjective Data i. Related to infection and liver's inability to function normally. 1. Chills 2. Complaints of dull abdominal pain 3. Abdominal tenderness 4. Discomfort r. Objective Data i. Related to infection and liver function. 1. Fever 2. Hepatomegaly 3. Jaundice 4. Anemia 5. Clay-colored stools 6. Dark urine s. Diagnostic Tests i. Ultrasound ii. CT iii. Liver scan iv. Liver biopsy v. Bilirubin levels vi. Liver enzymes vii. Blood cultures viii. CBC t. Medical Management i. IV antibiotic therapy ii. Percutaneous drainage iii. Open surgical drainage u. Nursing Implications i. Continuous monitoring and supportive care of patient's condition ii. Monitoring symptoms iii. Notify HCP if signs and symptoms increase in severity. v. Patient Problems and interventions for the patient with a liver abscess. i. In addition to the relationship of infection and nutrition a. Teach preoperative and postoperative procedures. b. Assess patient's understanding. ii. Prognosis c. Sepsis was commonly the cause of death. d. Advanced diagnostic (CT and liver scans) has improved patient outcomes. 1. Gallbladder -- a pear-shaped organ measuring approximately 7-10 cm (3-4 inches) long. Areolar connective tissue connects it to the underside of the liver. 2. It can store 30 to 50 mL of bile and its primary function is to store and eject bile into the duodenum for digestion of fats. 38. The gallbladder is an accessory digestive organ which is in the right upper quadrant of the abdominal cavity. a. Cholelithiasis: *formation of stones in the gallbladder* (gallstones). These stones may be as small as a grain of sand, and may become as large as an inch in diameter. 3. Incidence of Cholelithiasis: a. Seen more common in women than men. b. Occurs more f requently in Native Americans, c. Seen more commonly in obese persons, pregnant women, women with a history of multiple pregnancies, use of birth control pills and diabetics. 4. Causes of Cholecystitis: (Inf lammation of the gallbladder) d. Obstruction, gallstone or tumor. e. Lipid metabolism and female sex hormones play f. Cause of gallstone formation is unknown. 5. Clinical Manifestations: g. Acute: indigestion, nausea, vomiting with severe, colicky pain in the right upper quadrant. Pain may be referred to the right shoulder and scapula. h. Chronic: several mild attacks of pain and i. Pain is often mistaken for a cardiac problem because of the pain that is felt in the epigastric region and radiating to the back. \[Instructor recommendation- Ask students why they pain is mistaken for cardiac problem before offering explanation.\] ---------------------------------------------------------------------------------------------------------------------- 6. Assessment: j. Subjective: i. Indigestion after eating high fatty foods. ii. Acute pain may have an abrupt onset and iii. Pain localizes in the right upper-quadrant iv. May radiate around the mid-torso to the v. Anorexia, nausea, vomiting and f latulence. vi. May experience tachycardia and tachypnea with diaphoresis (may lead patient to believe he/she is experiencing an MI). vii. Symptoms are decreased or absent in those with chronic cholecystitis. k. Objective: viii. Low-grade fever with leukocytosis ix. Tachycardia and tachypnea. x. Mild jaundice. xi. Fatty stools (steatorrhea), and clay- colored stools caused by lack of bile in the intestinal tract. xii. Dark amber or tea colored urine (contains xiii. Nausea/vomiting l. Diagnosis: xiv. based on the history, physical examination, xv. Fecal studies: reveal decreased bile xvi. Serum bilirubin tests: reveal elevated m. Radiographic studies: xvii. Ultrasound of the gallbladder and biliary system: to identify stones. xviii. Cholecystograms. iv. Cholangiography. v. ERCP. vi. MRI/CT scan. vii. HIDA Scan n. Medical Management: xix. Chronic Attack: treated with a low xx. Mild Cholelithiasis: conservative xxi. Bedrest. xxii. NG tube to low suction. xxiii. NPO: allows GI tract and gallbladder to xxiv. IV f luids to maintain hydration and replace xxv. Pain control: Demerol (drug of choice, because of decreased incidence of spasms to sphincter of Oddi). NOT Morphine! xxvi. Antibiotics: 1. Prophylactically. 2. To treat a current infection. 3. After gallbladder perforation, if it xxvii. Extracorporeal Shock Wave Lithotripsy (ESWL): 4. Used to treat a patient who has mild or moderate symptoms caused by few stones. 5. Machine discharges a series of shockwaves through water or a cushion that breaks the stone into f ragments. 6. Natural f low of bile carries the stones out of the 4. For stones in the common bile duct: a. Endoscopic Sphincterotomy: a f lexible endoscope is b. The stone is snared or retrieved using a basket-like o. Nursing Management (patient treated medically for cholelithiasis): +-----------------------+-----------------------+-----------------------+ | | | 1. 2. | +-----------------------+-----------------------+-----------------------+ | | | 1. 2. 3. 4. 5. 6 | | | |. | +-----------------------+-----------------------+-----------------------+ | | | 1. 2. | +-----------------------+-----------------------+-----------------------+ | | | 1. | | | | | | | | | | | | | | | | 2. | | | | | | | | | | | | | | | | 3. 4. 5. | +-----------------------+-----------------------+-----------------------+ i. Surgical Management: Cholecystectomy and Laparoscopic Cholecystectomy. 1. Laparoscopic Cholecystectomy: a. Treatment of choice 80 to 85% of time. b. Narrow instruments including a camera are introduced into the abdomen through four small puncture holes. c. The gallbladder is found, the vessels and tubes are cut and the gallbladder is removed. d. ***Preferred treatment:*** 1. Less invasive, with shorter healing and recovery time. 2. No invasive scar. 3. Less pain with more rapid return to normal activities. e. Nursing Interventions (post-operative Laparoscopic Cholecystectomy): 4. Give oral analgesics or anti-inflammatory agents to relieve symptoms. 5. Oral liquids and light dinner post-operatively. 6. Provide anti-emetics, as needed. 7. Routine VS, report abnormal values. 8. Observe IV infusions for patency 9. Measure I & O and describe carefully. 10. Observe patient for complications e.g. hemorrhage, elevated temperature, and wound infection 11. Ambulate patient f irst night. a. Most patients are discharged the next day and resume moderate activity within 48 to 72 hours. b. One out of six patients is discharged the same day. 12. Patient Teaching: c. Assess patient\'s ability to eat and walk. d. Assess for abdominal distention, evidence of bleeding or bile leakage. e. Teach/assess understanding of conditions to report to physician: severe pain tenderness in right upper quadrant increase in abdominal girth, leakage from puncture site, increase in pulse. f. Patients can return to work in 3 days and full activity in 1 week. 2. Nursing Interventions: perform routine postsurgical assessments when the patient returns from surgery. 1. Examine drainage often for exudate or hemorrhage. 2. Notify surgeon if incision drainage is excessive (\>50 ml/8hrs), contains bile or is bright red. 3. Advance diet slowly. a. Leave NG tube clamped f rom 2 hours before meal and 2 hours after to aid in digestion. b. Open clamp if patient complains of nausea, abdominal pain, vomiting. 4. Observe for complications: c. Jaundice (f rom clogged common bile duct). d. Hemorrhage (decreased BP, urine output, increased pulse, visible bleeding). e. Peritonitis, wound infection, fever. +-----------------------+-----------------------+-----------------------+ | | | 1. | | | | | | | | | | | | | | | | 2. 3. 4. 5. | +-----------------------+-----------------------+-----------------------+ | | | 1. | | | | | | | | | | | | | | | | 2. 3. 4. 5. | +-----------------------+-----------------------+-----------------------+ | | | 1. 2. 3. 4. | +-----------------------+-----------------------+-----------------------+ | | | 1. 2. 3. | | | | | | | | | | | | | | | | 4. 5. | +-----------------------+-----------------------+-----------------------+ -- -- -- -- -- -- h. Patient teaching for post-operative patient: 1. Instruct post-surgical patient to try small amounts of foods that previously caused discomfort and gradually eliminate those that continue to do so. May usually resume normal diet. 2. Instruct patient to contact physician immediately if severe pain, jaundice, or fever occurs or if the color of the stools or urine changes. 1. Prompt treatment provides excellent prognosis. 2. Complications f rom cholecystectomy severely decreased since introduction of laparoscopic procedure. 3. Poorer prognosis with development of pancreatitis. 5. Learning Step / Activity 6. **Pancreatitis**. b. Etiology / Pathophysiology: Classified as acute or chronic. 7. Inf lammation of the pancreas, ranging f rom mild edema and inf lammation to enzymatic digestion of the pancreas, extensive hemorrhage, and necrosis. 8. In the pathophysiologic process of pancreatitis, the enzymes cannot f low out of the pancreas because of occlusion (an obstruction or closing off) of the pancreatic duct (Duct of Wirsung) by edema, stones, or scar tissue 9. Pancreas becomes inf lamed when there is reflux of bile and duodenal contents into the pancreatic duct, causing swelling and obstruction. 10. Pancreas begins to digest itself (autodigestion) with its own enzymes (especially Trypsin) 11. Trapped enzymes begin to act on the pancreas itself. 12. Causes: p. Structural/vascular abnormalities q. Trauma or disruption of the pancreatic ducts r. Infectious disease s. Metabolic disorders (hyperlipidemia and hypercalcemia) t. Inf lammatory bowel disease (f ) Heredity g. Excessive alcohol intake and certain drugs h. Re-feeding after prolonged fasting or anorexia. i. Many people who have no other illnesses may develop acute pancreatitis. c. Clinical Manifestations: 13. Severe abdominal pain which radiates up the back (LUQ). 14. Pain is relieved by sitting forward (taking pressure off the pancreas) 15. Jaundice may be noted if the bile duct is obstructed. d. Assessment: 16. Most common: severe upper abdominal pain, which can but not in all cases, radiate to both sides and straight through the back. 17. Nausea, vomiting and low-grade fever. 18. Hypotension. 19. Jaundice. 20. Bowel sounds may be diminished, with abdominal distention and tenderness. e. Diagnosis: 21. Abdominal CT/Ultrasound 22. Endoscopy 23. Pancreatic enzymes in the serum and urine 24. Serum **amylase** and **lipase** are 3 times above normal. Considered most 25. Leukocytosis, 26. Elevated hematocrit level 27. Hypocalcemia 28. Hypoalbuminemia 29. Hyperglycemia 11. ERCP (Endoscopic Retrograde Cholangiopancreatography). a. Used to evaluate obstructive jaundice b. Remove common bile duct stones c. Place biliary and pancreatic duct stents. f. Medical Management: 30. Measures taken to relieve pain and spasms (cause an increase in pancreatic secretions). u. Usually NPO, with NG tube to low continuous suction to relieve distention, N/V and reduce stimulation of pancreas to release juices. v. Analgesics may be prescribed and combined with antispasmodics to achieve optimal pain relief. w. Parenteral anticholinergic medication, such as atropine or propantheline, helps decrease pancreatic activity. Is contraindicated in paralytic x. Antacids or antihistamine H2 Receptor blockers such as cimetidine may be given to prevent stress ulcers caused by decreased gastric pH. y. Antibiotics may be given to treat a secondary infection. (f ) Cholecystectomy for gallstone pancreatitis. g. Clear liquid diet with gradual progression once pain is under control for 24 h. Low fat, low protein diet. No alcohol or caffeine. 31. Restore f luid and electrolyte losses: z. IV f luids. a. Albumin may be given IV to pull f luid trapped in peritoneum back into circulation. 32. Prevent or treat systemic complications, i.e., respiratory distress syndrome, b. Antibiotics (IV) to prevent localized abscesses and/or systemic sepsis. c. Percutaneous needle aspiration to treat pseudocysts. d. Patient may require debridement of necrotic tissue every 2 to 3 days. 1. Multiple drains may be placed in the abdomen to drain f luid and debris. 2. Continuous irrigation may be performed. f. Complications can occur with mild, acute, chronic, or severe pancreatitis. 6. Learning Step / Activity 7. **Pancreatic Cancer**. a. Pancreatic Cancer - A major factor in the high death rate f rom pancreatic cancer is the difficulty in diagnosing it at an early, curable stage. b. Etiology and Pathophysiology: The most common environmental risk factor for pancreatic cancer is cigarette smoking. c. Risk Factors: ------------- 1. Smoking is seen in 30% of patients. 2. Exposure to chemical carcinogens 3. Diabetes mellitus 4. Cirrhosis 5. Chronic pancreatitis 6. Diets high in red meat, pork and processed meat such as bacon 7. Coffee 8. Obesity 9. Genetics 10. African American male d. Etiology/Pathophysiology 1. The cancer may originate in the pancreas or be the result of metastasis f rom cancer of the lung, the stomach, the duodenum, or the common bile duct. 2. Most often the head of the pancreas is involved often and causes jaundice by compressing and obstructing the common bile duct. 3. As the cancer spreads, it may invade the posterior wall of the stomach, the duodenal wall, the colon, and the common bile duct. 4. Biliary obstruction and gallbladder dilation are subsequent complications. 5. It is not uncommon for the tumor to grow rapidly and invade the vascular and lymphatic system. Most patients only live 4 -- 6 months after diagnosis due to late diagnosis. e. Clinical Manifestations 1. Insidious onset of the disease with initially vague symptoms generally accounts for delays in diagnosis. 2. Complaints of anorexia, malaise, nausea, and fatigue 3. Abdominal pain in the mid-epigastric region or back occurs in many of the patients 4. About half the patients will develop diabetes mellitus if islet cells are involved. f. Assessment 1. A psychosocial history is taken; it may reveal that the patient belongs to one of the at-risk populations such as cigarette smokers, coal- and gas-plant employees, chemists, and workers exposed to beta-naphthol and benzidine. 2. Subjective data includes: anorexia, fatigue, nausea, f latulence, a change in stools, and steady, dull, and aching pain in the epigastrium or referred to the back 3. Objective data includes: weight loss (often gradual and progressive) 4. Jaundice f. Onset of diabetes mellitus (f ) Diagnostic Tests 1. Transabdominal ultrasound and CT 2. Endoscopic ultrasound with f ine needle biopsy 3. ERCP 4. Tumor markers g. Medical Management 1. Often malignant tumors of the pancreas are inoperable by the time they are diagnosed. 2. Treatment is primarily surgical and has been associated with a high mortality rate. 3. Surgical Treatments a. Cancer of the head of the pancreas is treated by pancreatoduodenectomy b. The Whipple procedure involves resection of the antrum of the stomach, the gallbladder, the duodenum, and varying amounts of the pancreas. Total pancreatectomy with resection of parts of the GI Tract c. Subtotal pancreatic resection has complications of postoperative pancreatic f istulas and is not recommended. h. Nursing Interventions and Patient Teaching 4. Care focuses on maintaining f luid and electrolyte balance, preventing hemorrhage, preventing respiratory complications, and monitoring endocrine and exocrine functions of the pancreas. 5. Palliative care is crucial for the patient and the family 6. The patient may receive long-acting narcotic analgesics and quick-acting opioids. 7. Offer compassionate care and emotional assistance i. Prognosis a. This is a lif e-threatening illness. b. Prognosis is very poor because of late diagnosis c. Median survival after diagnosis is only 5 to 12 months d. Exocrine pancreatic cancer has a low 5-years survival rate e. Prognosis is related to the tumor's location and the stage as which the disease is diagnosed. 1. Determine presence and location of pain. 2. Keep patient as comfortable as possible through the administration of analgesics and antispasmodic medications. 3. Ensure bed rest with bathroom privileges as ordered to reduce f low of pancreatic enzymes. 4. Nutritional needs are met by enteral feeding via jejunum as long as necessary. 5. Protect patient f rom injury, supportive care for patient and family. 6. Carefully monitor all replacement f luids and medications for proper administration. 7. Patient remains on a low fat, high-calorie, high-carbohydrate diet after discharge. 8. Alcohol and caffeinated beverages should be avoided +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. | | | | | | | | | | | | 5. 6. 7. | +-----------------------------------+-----------------------------------+ | | 1. 2. 3. 4. 5. | +-----------------------------------+-----------------------------------+ | | 1. Assess for S/S of fluid | | | volume deficit: decreased | | | level of consciousness, poor | | | skin turgor, cool, dry or | | | clammy skin, weak peripheral | | | pulses, edema formation. | | | | | | 2. 3. 4. Monitor VS, shock is | | | often an outstanding symptom | | | of acute pancreatitis. | +-----------------------------------+-----------------------------------+ | | 1. Maintain caloric intake | | | during NPO status with | | | prescribed glucose solution. | | | | | | 2. 3. 4. 5. 6. | +-----------------------------------+-----------------------------------+