Lola Oyedele MSN, RN, CTN Majuvy L. Sulse MSN, RN, CCRN

1. Liver and Biliary Lola Oyedele MSN, RN, CTN Majuvy L. Sulse MSN, RN, CCRN Pancreatic Problems NRS 108

2. LIVER • Largest organ excluding skin located RUQ • Lobule is functional unit • Fat, CHO, Protein metabolism • Clotting • Drug metabolism & detoxification • Liver enzymes • Alamine Aminotransferase • ALT, SGPT-5-35U/L • Aspartate Aminotransferase • AST, SGOT 0-35U/L • Alkaline Phosphatase • ALP 20-90U/L

3. Liver • Aminotransferases • Found in hepatocytes • Markers of liver cell injury • Detected within hours of injury to liver • AST used in conjunction with ALT • AST elevated in cardiac/skeletal muscle • Laboratory tests • PT/PTT • Se Albumin • Se Ammonia • Se Bilirubin • Conjugated-Direct, post hepatic, glucoronic acid • Unconjugated- indirect, pre hepatic,albumin bound • Urobilinogen-sensitive test for hepatic damage

4. Liver Biopsy • Pre procedure • Needle between 6-7 or 8-9th intercostals • Check coagulation • Type & X-match • Baseline VS • Sustained exhalations- prevent lung injury • consent • Post procedure • VS • Lie on R side for 2 hours • Flat 12-14 hours • Watch for complications-shock, R pneumothorax, Biliary peritonitis (rigid abdomen, high temp)

5. Jaundice • Yellowish discoloration from bilirubin & breakdown of Hgb • Normal 2-3MG/DL (jaundice 3-4x normal value) • Sclera & skin, palm of hands/feet • Hemolytic • Increased RBC breakdown • Increased unconjugated bilirubin • Hemolytic anemia, ABO incompatibility • Hepatocellular • Liver unable to take up bilirubin • Conjugated & excreted • Cirrhosis • Obstructive • Impeded or obstructive • Intrahepatic- swelling, fibrosis, tumors, cirrhosis, hepatitis • Extrahepatic-CBD stones, Ca pancreas

6. CIRRHOSIS • DESCRIPTION • A chronic, progressive disease of the liver, characterized by diffuse damage to cells with fibrosis and nodular regeneration • Repeated destruction of hepatic cells causes the formation of scar tissue-nodular • ASSESSMENT • Anorexia and weight loss • Early morning nausea and vomiting (presence of blood in vomitus) • Dyspepsia • Flatulence and changes in bowel habits • Emaciation • Fatigue

7. CIRRHOSIS • Hepatomegaly • Protruding umbilicus • Dilated abdominal veins • Fetor hepaticus; the fruity, musty breath odor of chronic liver disease • Asterixis (liver flap): A course tremor characterized by rapid, nonrhythmic extension and flexions in the wrist and fingers • Delirium • ASSESSMENT • Jaundice • Abdominal pain or tenderness • Ascites • Peripheral edema • Dry skin and rashes • Petechiae or ecchymosis • Spider angiomas on the nose, cheeks, upper thorax, and shoulders

8. TYPES OF CIRRHOSIS • LAENNEC'S CIRRHOSIS • Alcohol-induced, nutritional, or portal cirrhosis • Cellular necrosis causes eventual widespread scar tissue, with fibrotic infiltration of the liver • POSTNECROTIC CIRRHOSIS • Occurs after massive liver necrosis • Results as a complication of acute viral hepatitis or exposure to hepatotoxins • Scar tissue causes destruction of liver lobules and entire lobes

9. TYPES OF CIRRHOSIS • BILIARY CIRRHOSIS • Develops from chronic biliary obstruction (secondary), bile stasis (Primary), and inflammation resulting in severe obstructive jaundice • CARDIAC CIRRHOSIS • Associated with severe, right-sided congestive heart failure (CHF) and results in an enlarged, edematous, congested liver • The liver becomes anoxic, resulting in liver cell necrosis and fibrosis

10. COMPLICATIONS OF CIRRHOSIS • PORTAL HYPERTENSION • A persistent increase in pressure within the portal vein that develops as a result of obstruction to flow of blood • Causes splenomegaly as blood backs up • Also results in ascites, esophageal varices & hemorrhoids

11. COMPLICATIONS OF CIRRHOSIS • ASCITES • The accumulation of fluid (plasma)within the peritoneal cavity that results in venous congestion of the hepatic capillaries • Increased hydrostatic pressure leads to plasma leaking directly from the liver surface and portal vein • Increased hepatic lymph formation present • Renal vasoconstriction-triggers RAS-causes water & Na reabsorption

12. ASCITES • Treatment • Non surgical management • Diet • Drug • Comfort measures • Paracentesis • Surgical management • Shunt • Peritoneovenous(LeVeen shunt) • Denver shunt

13. COMPLICATIONS OF CIRRHOSIS • BLEEDING ESOPHAGEAL VARICES • Fragile, thin-walled, distended esophageal veins that become irritated and rupture • Caused by-chemical irritant, mechanical trauma, increased pressure from esophagus & stomach • Treatment- • Esophageal tamponade • Gastric decompression & lavage • Vasopressin • Endoscopic sclerotherapy or ligation • TIPS

14. COMPLICATIONS OF CIRRHOSIS • JAUNDICE • Occurs because the liver is unable to metabolize bilirubin and because the edema, fibrosis, and scarring of the hepatic bile ducts interfere with normal bile and bilirubin secretion • PORTAL SYSTEMIC ENCEPHALOPATHY • End stage hepatic failure and cirrhosis, characterized by altered LOC, neurological symptoms, impaired thinking, and neuromuscular disturbances

15. Encephalopathy • Stages of encephalopathy • Stage 1- • mild confusion, forgetfulness, mood changes, irritability, sleep disturbance • Stage 2 • lethargy • Aberrant behavior • Liver flaps • Stage 3 • Severe confusion-violent behavior • Speech mumbling, asterixis • hyperventilation • Stage 4 • Comatose • Abnormal posturing • EEg abnormal

16. Management of Encephalopathy • Identify & treat cause • GI bleed, systemic infection, drugs, alkalosis, dehydration • Eliminate or reduce generation of Ammonia toxins • Control intake<0.5G/Kg/Day • Calories 35-40KCAL/Kg/Day <Tyrosine/Phenylalanine,> Leucine/Valine • Vit A,D,E, K • Reduce amount of bacteria in bowel • Stop Nitrogen containing drugs, give Neomycin, Lactulose, Magnesium Citrate, fiber, stool softener, enemas • Hasten movement of ammonia in the bowel-3-5x stools/day • Lactulose

17. COMPLICATIONS OF CIRRHOSIS • HEPATORENAL SYNDROME • Progressive renal failure associated with hepatic failure • Characterized by a sudden decrease in urinary output, elevated blood urea nitrogen (BUN) and creatinine, decreased urine sodium excretion, and increased urine osmolarity • COAGULATION DEFECTS • Decreased synthesis of bile fats in the liver prevent the absorption of fat-soluble vitamins • Without vitamin K and clotting factors II, VII, IX, and X, the client is prone to bleeding

18. CIRRHOSIS • IMPLEMENTATION • Elevate the head of the bed to minimize shortness of breath • If ascites and edema is absent and the client does not exhibit signs of impending coma, a high-protein diet supplemented with vitamins is prescribed • Provide supplemental vitamins (B complex, vitamin A, C, and K, folic acid, and thiamine) as prescribed • Restrict sodium intake and fluid intake as prescribed • Initiate enteral feedings or TPN as prescribed • Administer diuretics as prescribed • Monitor I&O and electrolyte balance • Weigh client and measure abdominal girth daily • Monitor LOC; assess for precoma state (tremors, delirium)

19. CIRRHOSIS • IMPLEMENTATION • Monitor for asterixis • Maintain gastric intubation to assess bleeding and/or esophagogastric balloon tamponade to control bleeding varices if prescribed • Administer blood products as prescribed • Monitor coagulation laboratory results; administer vitamin K if prescribed • Administer low-sodium antacids as prescribed • Administer Lactulose (Chronulac), which decreases the pH of the bowel, decreases production of ammonia by bacteria in the bowel, and facilitates the excretion of ammonia

20. CIRRHOSIS • Administer neomycin (Mycifradin) as prescribed to inhibit protein synthesis in bacteria and decrease the production of ammonia • Avoid medications such as narcotics, sedatives, and barbiturates, and any hepatotoxic medications or substances • Instruct the client about the restriction of alcohol intake • Prepare the client for paracentesis to remove abdominal fluid • Prepare the client for surgical shunting procedures if prescribed

21. Fatty Liver • Accumulations of triglycerides & fats in hepatic cells • Causes- alcoholism, malnutrition, DM, Obesity TPN, Pregnancy • S/S-RUQ pain, edema, hepatomegaly, jaundice • Dx-liver biopsy • Tx-dietary restrictions

22. Hepatic Abcess • Invasion of bacteria or protozoa-causing necrotic cavity filled with leukocytes & infective agents. • Causative agents- E Coli, Klebsiella, Salmonella, Enterococcus & Staph • Dx-liver scan • Labs-blood culture to detect organism

23. LIVER Cancer • Hepatocellular carcinoma- most common primary liver Ca • Metastatic Ca is more common than primary Ca • Malignant cells cause liver to be enlarged and mishapen • Difficult to diagnose • Clinical manifestations similar to cirrhosis • Tests used-CT, MRI, ERCP, liver biopsy, AFP (elevated in 70% of hepatocellular Ca & helps to distinguish primary from metastatic cancer • Cryosurgery- cryoprobes directly in liver-liquid nitrogen used to freeze liver tissue • Radiofrequency-electrical energy to create heat in specific location • PEI-percutaneous ethanol injection-guided US • chemotherapy • Liver transplantation

24. CHOLECYSTITIS • DESCRIPTION • An inflammation of the gallbladder that may occur as an acute or chronic process • Acute inflammation is associated with gallstones (cholelithiasis) • Chronic cholecystitis results when inefficient bile emptying and gallbladder muscle wall disease cause a fibrotic and contracted gallbladder • A calculus cholecystitis occurs in the absence of gallstones and is due to bacterial invasion via the lymphatic or vascular systems

25. CHOLECYSTITIS • ASSESSMENT • Nausea and vomiting • Indigestion, Belching, Flatulence • Epigastric pain that radiates to the scapula 2 to 4 hours after eating fatty foods and may persist for 4 to 6 hours • Pain localized in right upper quadrant • Guarding, rigidity, and rebound tenderness • Mass palpated in the right upper quadrant • Murphy’s sign (cannot take a deep breath when the examiner’s fingers are passed below the hepatic margin) • Elevated temperature, Tachycardia • Signs of dehydration • Jaundice, pruritus, dark orange and foamy urine • Steatorrhea and clay-colored feces

26. CHOLECYSTITIS • IMPLEMENTATION • Maintain NPO status during nausea and vomiting episodes • Maintain nasogastric decompression • Administer antiemetics • Administer analgesics as prescribed to relieve pain and reduce spasm (morphine sulfate or codeine sulfate may cause spasm of the sphincter of Oddi and increase pain) • Administer antispasmodic (anticholinergics) as prescribed to relax smooth muscle • Instruct the client with chronic cholecystitis to eat low-fat meals more frequently in small amounts • Instruct the client to avoid gas-forming foods • Prepare the client for nonsurgical and surgical procedures as prescribed

27. CHOLECYSTITISNONSURGICAL IMPLEMENTATION • DISSOLUTION THERAPY • To remove cholesterol stones • Chenodeoxycholic acid (Chenodiol) or ursodiol (Actigall) is administered PO to decrease the size of the stones or to dissolve small stones • Direct contact with repeated injections and aspirations of a dissolution agent via percutaneous catheter may be performed

28. CHOLECYSTITISNONSURGICAL IMPLEMENTATION • EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY • Shock waves are administered that disintegrate stones in the biliary system • Oral dissolution follows

29. CHOLECYSTITISSURGICAL IMPLEMENTATION • CHOLECYSTECTOMY • Removal of the gallbladder • CHOLEDOCHOTOMY • Incision into the common bile duct to remove the stone • Surgical procedures may be performed by laparoscopy

30. CHOLECYSTITIS • POSTOPERATIVE IMPLEMENTATION • Monitor for respiratory complications secondary to pain at the incisional site • Encourage coughing, deep breathing & early ambulation • Splinting the abdomen to prevent discomfort during coughing • Administer antiemetics as prescribed for nausea and vomiting • Administer analgesics as prescribed for pain relief • Maintain NPO status and NG tube suction as prescribed • Advance diet from clear liquids to solids when prescribed and as tolerated by the client • Maintain and monitor drainage from the T-tube, if present

31. PANCREATITIS • DESCRIPTION • An acute or chronic inflammation of the pancreas with associated escape of pancreatic enzymes into surrounding tissue • Acute pancreatitis occurs suddenly as one attack or can be recurrent, but resolves • Chronic pancreatitis is a continual inflammation and destruction of the pancreas, with scar tissue replacing pancreatic tissue • Precipitating factors: • trauma, alcohol, biliary tract disease, viral or bacterial disease, hyperlipedemia, hypercalcemia, cholelithiasis, hyperparathyroidism, ischemic vascular disease, and peptic ulcer disease

32. ACUTE PANCREATITIS • ASSESSMENT • Abdominal pain, including a sudden onset at the mid-epigastric or left upper quadrant location with radiation to the back • Pain that is aggravated by a fatty meal, alcohol, or lying in a recumbent position • Abdominal tenderness and guarding • Nausea and vomiting • Weight loss • Cullen’s sign (discoloration of the abdomen and periumbilical area) • Turner’s sign (bluish discoloration of the flanks) • Absent or decreased bowel sounds • Elevated WBC, glucose, bilirubin, alkaline phosphatase, urinary amylase • Elevated lipase and amylase

33. CULLEN’S SIGN VS TURNER’S SIGN

34. ACUTE PANCREATITIS • IMPLEMENTATION • Maintain NPO status and maintain hydration with IV fluids as prescribed • Administer TPN for severe nutritional depletion • Administer supplemental preparations and vitamins and minerals to increase caloric intake if prescribed • Maintain NG tube to decrease gastric distention and suppress pancreatic secretion • Administer meperidine hydrochloride (Demerol) as prescribed for pain because it causes less incidence of smooth muscle spasm of the pancreatic ducts and sphincter of Oddi (avoid morphine sulfate or codeine sulfate, which may cause spasms) • Administer antacids as prescribed to neutralize gastric secretions

35. ACUTE PANCREATITIS • IMPLEMENTATION • Administer histamine H2-receptor antagonists as prescribed to decrease hydrochloric acid production and prevent activation of pancreatic enzymes • Administer anticholinergics as prescribed to decrease vagal stimulation, decrease GI motility, and inhibit pancreatic enzyme secretion

36. ACUTE PANCREATITIS • CLIENT EDUCATION • The importance of avoiding alcohol • The importance of follow-up visits with the physician • To notify the physician if acute abdominal pain, jaundice, clay-colored stools, or dark urine develops

37. CHRONIC PANCREATITIS • ASSESSMENT • Abdominal pain and tenderness • Left upper quadrant mass • Steatorrhea and foul-smelling stools that may increase in volume as pancreatic insufficiency increases • Weight loss • Muscle wasting • Jaundice • Signs and symptoms of diabetes mellitus

38. CHRONIC PANCREATITIS • IMPLEMENTATION • Provide supplemental preparations and vitamins and minerals to increase caloric intake • Administer pancreatic enzymes as prescribed to aid in the digestion and absorption of fat and protein • Administer insulin or oral hypoglycemic medications as prescribed to control diabetes mellitus, if present

39. CHRONIC PANCREATITIS • CLIENT EDUCATION • The prescribed dietary measures (fat and/or protein intake may be limited) • Avoid heavy meals • The importance of avoiding alcohol • The use of pancreatic enzyme medications • The treatment plan for glucose management • To notify the physician if increased steatorrhea occurs or if abdominal distention or cramping, and skin breakdown develops • The importance of follow-up visits

40. HEPATITIS • DESCRIPTION • An inflammation of the liver caused by a virus, bacteria, or exposure to medications or hepatotoxins • The goals of treatment include resting the inflammed liver to reduce metabolic demands and increasing the blood supply, thus promoting cellular regeneration and preventing complications

41. STAGES OF VIRAL HEPATITIS • PREICTERIC STAGE • The first stage of hepatitis preceding the appearance of jaundice • Flu-like symptoms: malaise, fatigue • Anorexia, nausea, vomiting, diarrhea • Pain: headache, muscle aches, polyarthritis • Serum bilirubin and enzyme levels are elevated

42. STAGES OF VIRAL HEPATITIS • ICTERIC STAGE • The second stage of hepatitis, which includes the appearance of jaundice and associated symptoms such as elevated bilirubin levels, dark or tea-colored urine, and clay-colored stools • Jaundice • Pruritus • Brown-colored urine • Lighter-colored stools • Decrease in preicteric phase symptoms

43. STAGES OF VIRAL HEPATITIS • POSTICTERIC STAGE • The convalescent stage in which the jaundice decreases and the color of the urine and stool return to normal • Energy levels increase • Pain subsides • GI symptoms are minimal to absent • Serum bilirubin and enzyme levels return to normal

44. VIRAL HEPATITISLABORATORY ASSESSMENT • ALANINE AMINOTRANSFERASE (ALT) • Elevated to more than 1000 mU/ml and may rise to as high as 4000 mU/ml • Normal adult blood value: 6 to 24 U/L • ASPARTATE AMINOTRANSFERASE (AST) • May rise to 1000 to 2000 mU/ml • Normal adult blood value: 8 to 26 U/L • ALKALINE PHOSPHATASE LEVELS • May be normal or mildly elevated • Normal adult blood value: 4.5 to 13 King-Armstrong units/dl • SERUM TOTAL BILIRUBIN LEVELS • Elevated to greater than 2.5 mg/dl • Normal: less than 1.5 mg/dl • Elevated levels of bilirubin in the urine

45. HEPATITIS A (HAV) • DESCRIPTION • Formerly known as infectious hepatitis • Commonly seen during the fall and early winter • INCREASED RISK INDIVIDUALS • Commonly seen in young children • Individuals in institutionalized settings • Health care personnel

46. HEPATITIS A (HAV) • TRANSMISSION • Fecal-oral route • Person-to-person contact • Parenteral • Contaminated fruits, vegetables, or uncooked shellfish • Contaminated water or milk • Poorly washed utensils • INCUBATION PERIOD • 2 to 6 weeks • INFECTIOUS PERIOD • 2 to 3 weeks prior to, and 1 week after, developing jaundice • COMPLICATION • Fulminant hepatitis

47. HEPATITIS A (HAV) • PREVENTION • Strict handwashing • Stool and needle precautions • Treatment of municipal water supplies • Serologic screening of food handlers • Hepatitis A vaccine (Havrix) • Immune globulin (IG): For individuals exposed to HAV who have never received the hepatitis A vaccine; administer during the period of incubation and within 2 weeks of exposure • IG is recommended for household members and sexual contacts of individuals with Hepatitis A • Pre-exposure prophylaxis with IG is recommended for individuals traveling to countries with poor or uncertain sanitation conditions

48. HEPATITIS B (HBV) • DESCRIPTION • Is nonseasonal in nature • All age groups are affected • INCREASED RISK INDIVIDUALS • Drug addicts • Clients undergoing long-term hemodialysis • Health care personnel

49. HEPATITIS B (HBV) • TRANSMISSION • Blood or body fluid contact • Infected blood products • Infected saliva or semen • Contaminated needles • Sexual contact • Parenteral • Perinatal period • Blood or body fluids contact at birth

50. HEPATITIS B (HBV) • INCUBATION PERIOD • 6 to 24 weeks • COMPLICATIONS • Fulminant hepatitis • Chronic liver disease • Cirrhosis • Primary hepatocellular carcinoma