1. Cirrhosis of the Liver and Liver Failure Developed by Cheryl McConnell RN MSN

2. Pathophysiology Slow, insidious, progressive, chronic Slow, insidious, progressive, chronic Fibrous bands replace normal liver structure Fibrous bands replace normal liver structure Cell degeneration occurs Cell degeneration occurs Liver attempts to regenerate cells but cells are abnormal and disorganized Liver attempts to regenerate cells but cells are abnormal and disorganized Causes abnormal blood and lymph flow Causes abnormal blood and lymph flow Results in more fibrous tissue formation Results in more fibrous tissue formation

3. Normal Liver

4. Incidence of Cirrhosis Tenth leading cause of death in US Tenth leading cause of death in US At least 25,000 deaths annually At least 25,000 deaths annually Higher death rates for men than women Higher death rates for men than women  mortality in African Americans and Hispanics  mortality in African Americans and Hispanics

6. Types of Cirrhosis Laennec’s (alcoholic) Laennec’s (alcoholic) Postnecrotic Postnecrotic Biliary Biliary Cardiac Cardiac

9. Laennec’s Cirrhosis Most common type of cirrhosis Most common type of cirrhosis Also called alcoholic or portal Also called alcoholic or portal Alcohol causes inflammation to liver cells Alcohol causes inflammation to liver cells Leads to fatty deposits and hepatomegaly Leads to fatty deposits and hepatomegaly Scarring formed and liver cells destroyed Scarring formed and liver cells destroyed Malnutrition and more alcohol accelerate the damage Malnutrition and more alcohol accelerate the damage

11. Postnecrotic Cirrhosis Caused by viral hepatitis or hepatotoxins Caused by viral hepatitis or hepatotoxins Scar tissue destroys liver lobes Scar tissue destroys liver lobes Liver initially enlarges but then shrinks in size Liver initially enlarges but then shrinks in size 10 – 30% of all cirrhoses 10 – 30% of all cirrhoses

13. Biliary Cirrhosis Caused by chronic biliary obstruction or stasis of bile, biliary inflammation, or hepatic fibrosis Caused by chronic biliary obstruction or stasis of bile, biliary inflammation, or hepatic fibrosis Excessive bile leads to liver cell destruction and formation of nodules in the lobes Excessive bile leads to liver cell destruction and formation of nodules in the lobes 5 – 10% of all cirrhoses 5 – 10% of all cirrhoses

14. Cardiac Cirrhosis Seen with right sided heart failure Seen with right sided heart failure Liver is engorged with venous blood Liver is engorged with venous blood Becomes enlarged, edematous, and dark Becomes enlarged, edematous, and dark Venous congestion results in anoxia Venous congestion results in anoxia Cell necrosis results Cell necrosis results

23. Diagnostic Data  AST, ALT, LDH, Alk phos  AST, ALT, LDH, Alk phos  bilirubin, ammonia,  bilirubin, ammonia,  coagulation studies  coagulation studies Serum protein levels depend on disease Serum protein levels depend on disease  with acute liver disease  with acute liver disease  with chronic liver disease  with chronic liver disease

24. More Diagnostics Abdominal x-ray Abdominal x-ray Upper GI series Upper GI series Angiography Angiography Abdominal CT Abdominal CT EGD EGD Liver biopsy Liver biopsy Nuclear scan Nuclear scan

28. Signs and Symptoms Neurological Neurological AsterixisParaesthesias  LOCSensory disturbances Behavorial changesCognitive changes Behavorial changesCognitive changes  Skin Spider angiomasPalmar erythma JaundicePruitis  hair productioncaput medusa  pigmentationBruising White Nails

29. Caput Medusae

30. Spider Angiomas

31. Palmar Erythema

32. More Signs and Symptoms GI GI Abdominal painAnorexia AscitesDiarrhea Clay colored stoolsFetor hepaticus GastritisGI bleeding N/VVarices Malnutrition

33. “White Nails”

34. More Signs and Symptoms Cardiovascular Cardiovascular DysrhythmiasPortal hypertension Collateral circulationFatigue Peripheral edema Endocrine Endocrine Gynecomastia Amenorrhea Gynecomastia Amenorrhea  aldosterone, ADH, estrogens, glucocorticoids

35. More Signs and Symptoms Respiratory Respiratory DyspneaHypoxia Blood Blood AnemiaDIC Thrombocytopenia  WBCs HypokalemiaHypocalcemia Hypo/HypernatremiaHypomagnesia

37. More Signs and Symptoms Immune Immune  Susceptibility to infections Leukopenia  Renal  Urinary output

38. Complications Portal hypertension Portal hypertension Ascites Ascites Varices Varices Coagulation defects Coagulation defects Jaundice Jaundice PSE (portal systemic encephalopathy) PSE (portal systemic encephalopathy) Hepatorenal syndrome Hepatorenal syndrome

39. Portal Hypertension Increased pressure within the portal vein Increased pressure within the portal vein Results in obstruction of blood flow through the portal vein Results in obstruction of blood flow through the portal vein Blood tries to find new ways around obstructed area = collateral circulation Blood tries to find new ways around obstructed area = collateral circulation Causes venous distention in entire GI tract Causes venous distention in entire GI tract

40. Ascites Accumulation of plasma in the peritoneal cavity Accumulation of plasma in the peritoneal cavity Caused by increased pressure forcing fluid out of intravascular space into cavity Caused by increased pressure forcing fluid out of intravascular space into cavity Plasma contains albumin so circulating proteins decreased Plasma contains albumin so circulating proteins decreased  serum osmotic pressure  serum osmotic pressure Intravascular fluid depletion stimulates kidney to conserve sodium and water =  hydrostatic pressure and creates more ascites Intravascular fluid depletion stimulates kidney to conserve sodium and water =  hydrostatic pressure and creates more ascites

41. Ascites

42. Varices Occur anywhere in the GI tract especially Occur anywhere in the GI tract especially Esophageal Hemorrhoids Esophageal Hemorrhoids Bleeding esphageal varices Bleeding esphageal varices Caused by thin walled veins that are irritated, distended and eventually rupture Caused by thin walled veins that are irritated, distended and eventually rupture Chemical irritants Mechanical trauma  Esophagus pressure  Prone to hemorrhage – medical emergency

44. Esophageal Varices

45. Coagulation Defects Susceptible to bleeding Susceptible to bleeding Bruises easily Bruises easily Does not clot Does not clot Esophageal varices bleeding Esophageal varices bleeding

46. Jaundice Due to hepatocellular destruction or hepatic obstruction Due to hepatocellular destruction or hepatic obstruction Hepatocellular – cannot metabolize bilirubin so it builds up Hepatocellular – cannot metabolize bilirubin so it builds up Obstruction – clogs bile ducts so excretion is not possible Obstruction – clogs bile ducts so excretion is not possible

47. Jaundice

49. PSE PSE Also known as hepatic coma Also known as hepatic coma Seen in end stage hepatic failure Seen in end stage hepatic failure Can be insidious or rapid onset depending on the severity of liver disease Can be insidious or rapid onset depending on the severity of liver disease Caused by impaired ammonia metabolism Caused by impaired ammonia metabolism

50. PSE Continued Usually protein breaks down into ammonia in GI tract, then ammonia into urea --- excreted by the kidneys Usually protein breaks down into ammonia in GI tract, then ammonia into urea --- excreted by the kidneys Liver cannot convert ammonia into urea Liver cannot convert ammonia into urea Results in  serum ammonia levels Results in  serum ammonia levels Toxic to the central nervous system Toxic to the central nervous system

51. PSE Continued Other factors that add to PSE: Other factors that add to PSE: High protein diet Infection Hypovolemia Constipation GI bleeding Medications

52. Stages of PSE #1 - Prodomal – very subtle changes #1 - Prodomal – very subtle changes Personality/behavior changes Personality/behavior changes Impaired thinking/concentration Impaired thinking/concentration Emotional highs and lows Emotional highs and lows Fatigue, drowsiness Fatigue, drowsiness Slurred or slow speech Slurred or slow speech Sleep pattern disturbance Sleep pattern disturbance

53. Stages of PSE #2 – Impending #2 – Impending Continued mental deterioration Continued mental deterioration Confusion Confusion Disoriented Disoriented Asterixis Asterixis

54. Stages of PSE #3 – Stuporuous #3 – Stuporuous Marked mental confusion Marked mental confusion Drowsy but arousable Drowsy but arousable Abnormal EEG Abnormal EEG Muscle twitching Muscle twitching Hyperreflexia Hyperreflexia Continued asterixis Continued asterixis

55. Stages of PSE # 4 – Comatose (85% mortality rate) # 4 – Comatose (85% mortality rate) Unresponsive Unresponsive Responds to painful stimuli only Responds to painful stimuli only No asterixis No asterixis Positive Babinski’s sign Positive Babinski’s sign Muscle rigidity Muscle rigidity Fetor hepaticus Fetor hepaticus Seizures Seizures

56. Hepatorenal Syndrome A primary cause of death with hepatic failure/cirrhosis A primary cause of death with hepatic failure/cirrhosis Kidneys cannot excrete ammonia and bilirubin Kidneys cannot excrete ammonia and bilirubin Results in acute tubular necrosis Results in acute tubular necrosis Signs/symptoms Signs/symptoms Sudden  urinary output  BUN, Cr, urine osmolarity  Urine Na

57. Treatment Diet Diet  Sodium (< 2 grams)  Sodium (< 2 grams)  Carbohydrate, moderate fats  Carbohydrate, moderate fats  Protein  Protein Unless PSE present then  protein Unless PSE present then  protein Fluid restriction (total of ≤ 1500cc/day) Fluid restriction (total of ≤ 1500cc/day) Vitamin supplements Vitamin supplements

58. Treatment Continued Medications Medications Diuretics Diuretics Electrolyte replacement Electrolyte replacement Antacids Antacids Must be low sodium – Riopan Must be low sodium – Riopan Lactulose Lactulose Facilitates evaculation of ammonia Facilitates evaculation of ammonia Neomycin Neomycin Eliminates intestinal flora =  protein breakdown Eliminates intestinal flora =  protein breakdown Levadopa Levadopa For PSE – repairs damaged neurotransmitters For PSE – repairs damaged neurotransmitters

59. More Treatments Ascites control Ascites control Paracentesis Paracentesis Shunts Shunts Le Veen Shunt - drains ascites fluid into superior vena cava Le Veen Shunt - drains ascites fluid into superior vena cava Denver Shunt – subcutaneous pump that is manually compressed Denver Shunt – subcutaneous pump that is manually compressed Post op care: same as with any abdominal surgery, watch for fluid volume overload and bleeding disorders, measure abdominal girth every shift Post op care: same as with any abdominal surgery, watch for fluid volume overload and bleeding disorders, measure abdominal girth every shift

60. Le Veen Shunt

61. More Treatments Hemorrhage from varices Hemorrhage from varices Esophagogastric balloon tamponade Esophagogastric balloon tamponade Sengstaken-Blakemore tube – balloon inflates in esophagus and puts pressure on varices Sengstaken-Blakemore tube – balloon inflates in esophagus and puts pressure on varices Blood transfusions Blood transfusions Medications Medications Beta blockers to decrease HR and BP Beta blockers to decrease HR and BP Pitressin (vasopressin) IV or into superior mesenteric artery (via endoscopy) Pitressin (vasopressin) IV or into superior mesenteric artery (via endoscopy) Sclerotherapy Sclerotherapy Sclerosing agents injected into varices during EGD Sclerosing agents injected into varices during EGD Transjugular intrahepatic portal systemic shunt (TIPS) Transjugular intrahepatic portal systemic shunt (TIPS) Shunt between portal and hepatic vein to  pressure =  bleeding Shunt between portal and hepatic vein to  pressure =  bleeding Other portal system shunts – poor prognosis Other portal system shunts – poor prognosis

62. Sclerosing Procedure

63. Blakemore Tube

64. Another Blakemore Tube

65. More Treatments PSE PSE Low protein diet Low protein diet May need TPN May need TPN Control GI bleeding Control GI bleeding Medications Medications Neuro checks Neuro checks Look for signs and symptoms of the stages of PSE Look for signs and symptoms of the stages of PSE

66. Home Care Diet Diet  calories, vitamins, protein (unless PSE)  calories, vitamins, protein (unless PSE)  sodium  sodium Medications Medications Diurectics Diurectics Antacids, H2-receptor antagonists Antacids, H2-receptor antagonists No OTC medications No OTC medications No alcohol consumption No alcohol consumption  activity – rest periods  activity – rest periods Home care equipment Home care equipment

67. Evaluation Outcomes Patient will Patient will  in ascites  in ascites Electrolytes WNL Electrolytes WNL B/P WNL B/P WNL No bleeding or complications from bleeding No bleeding or complications from bleeding PSE managed immediatley PSE managed immediatley Optimal quality of life Optimal quality of life

68. EVOLUŢIE Ciroză compensată  ciroză decompensată vascular şi parenchimatos Rezerva funcţională – Clasificarea Child Pugh Parametru Albumina serică AscitaEncefalopatiaBilirubina Indicele Quick 1 pct. >3,5 AbsAbs < 2 > 70% 2 pct. 2,8-3,5Moderată Grd. I, II 2-340-70% 3 pct. < 2,8 Mare Grd. III, IV > 3 < 40% A: 5-6 pct., B: 7-9 pct., C: 10-15 pct.