1. Cirrhosis of the Liver (relates to Chapter 42, “Nursing Management: Liver, Biliary Tract, and Pancreas Problems,” in the textbook)

2. Description A chronic, progressive disease of the liver –Extensive parenchymal cell degeneration –Destruction of parenchymal cells A chronic, progressive disease of the liver –Extensive parenchymal cell degeneration –Destruction of parenchymal cells

3. Description Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis

4. Description Normal lobular structure distorted by fibrotic connective tissue Lobules are irregular in size and shape with impaired vascular flow Insidious, prolonged course Normal lobular structure distorted by fibrotic connective tissue Lobules are irregular in size and shape with impaired vascular flow Insidious, prolonged course

5. Statistics > 50% of liver disease in the US is directly related to alcohol consumption Of the estimated 15 million alcoholics in the USA 10-20% have or will develop cirrhosis > 50% of liver disease in the US is directly related to alcohol consumption Of the estimated 15 million alcoholics in the USA 10-20% have or will develop cirrhosis

6. Statistics Growing number of cases related to chronic hepatitis C 4th leading cause of death in people between 35 and 54 years of age Growing number of cases related to chronic hepatitis C 4th leading cause of death in people between 35 and 54 years of age

7. Statistics Direct correlation between alcohol consumption in any geographic area and the death rate from cirrhosis in that area

8. Etiology and Pathophysiology Cell necrosis occurs Destroyed liver cells are replaced by scar tissue Normal architecture becomes nodular Cell necrosis occurs Destroyed liver cells are replaced by scar tissue Normal architecture becomes nodular

9. Etiology and Pathophysiology Four types of cirrhosis: –Alcoholic (Laennec’s) cirrhosis –Postnecrotic cirrhosis –Biliary cirrhosis –Cardiac cirrhosis Four types of cirrhosis: –Alcoholic (Laennec’s) cirrhosis –Postnecrotic cirrhosis –Biliary cirrhosis –Cardiac cirrhosis

10. Etiology and Pathophysiology Alcoholic (Laennec’s) Cirrhosis –Associated with alcohol abuse –Preceded by a theoretically reversible fatty infiltration of the liver cells –Widespread scar formation Alcoholic (Laennec’s) Cirrhosis –Associated with alcohol abuse –Preceded by a theoretically reversible fatty infiltration of the liver cells –Widespread scar formation

11. Etiology and Pathophysiology Postnecrotic Cirrhosis –Complication of toxic or viral hepatitis –Accounts for 20% of the cases of cirrhosis –Broad bands of scar tissue form within the liver Postnecrotic Cirrhosis –Complication of toxic or viral hepatitis –Accounts for 20% of the cases of cirrhosis –Broad bands of scar tissue form within the liver

12. Etiology and Pathophysiology Biliary Cirrhosis –Associated with chronic biliary obstruction and infection –Accounts for 15% of all cases of cirrhosis Biliary Cirrhosis –Associated with chronic biliary obstruction and infection –Accounts for 15% of all cases of cirrhosis

13. Etiology and Pathophysiology Cardiac Cirrhosis –Results from longstanding severe right- sided heart failure Cardiac Cirrhosis –Results from longstanding severe right- sided heart failure

14. Manifestations of Liver Cirrhosis Fig. 42-5

15. Clinical Manifestations Early Manifestations Onset usually insidious GI disturbances: –Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits Onset usually insidious GI disturbances: –Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits

16. Clinical Manifestations Early Manifestations Abdominal pain Fever Lassitude Weight loss Enlarged liver or spleen Abdominal pain Fever Lassitude Weight loss Enlarged liver or spleen

17. Clinical Manifestations Late Manifestations Two causative mechanisms –Hepatocellular failure –Portal hypertension Two causative mechanisms –Hepatocellular failure –Portal hypertension

18. Clinical Manifestations Jaundice Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

19. Clinical Manifestations Jaundice Intermittent jaundice is characteristic of biliary cirrhosis Late stages of cirrhosis the patient will usually be jaundiced Intermittent jaundice is characteristic of biliary cirrhosis Late stages of cirrhosis the patient will usually be jaundiced

20. Clinical Manifestations Skin Spider angiomas (telangiectasia, spider nevi) Palmar erythema Spider angiomas (telangiectasia, spider nevi) Palmar erythema

21. Clinical Manifestations Endocrine Disturbances Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

22. Clinical Manifestations Endocrine Disturbances Alteration in hair distribution –Decreased amount of pubic hair –Axillary and pectoral alopecia Alteration in hair distribution –Decreased amount of pubic hair –Axillary and pectoral alopecia

23. Clinical Manifestations Hematologic Disorders Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

24. Clinical Manifestations Hematologic Disorders Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

25. Clinical Manifestations Peripheral Neuropathy Dietary deficiencies of thiamine, folic acid, and vitamin B 12

26. Complications Portal hypertension and esophageal varices Peripheral edema and ascites Hepatic encephalopathy Fetor hepaticus Portal hypertension and esophageal varices Peripheral edema and ascites Hepatic encephalopathy Fetor hepaticus

27. Complications Portal Hypertension Characterized by: –Increased venous pressure in portal circulation –Splenomegaly –Esophageal varices –Systemic hypertension Characterized by: –Increased venous pressure in portal circulation –Splenomegaly –Esophageal varices –Systemic hypertension

28. Complications Portal Hypertension Primary mechanism is the increased resistance to blood flow through the liver

29. Complications Portal Hypertension Splenomegaly Back pressure caused by portal hypertension  chronic passive congestion as a result of increased pressure in the splenic vein

30. Complications Portal Hypertension Esophageal Varices Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

31. Complications Portal Hypertension Esophageal Varices Varices have fragile vessel walls which bleed easily

32. Complications Portal Hypertension Internal Hemorrhoids Occurs because of the dilation of the mesenteric veins and rectal veins

33. Complications Portal Hypertension Caput Medusae Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

34. Complications Peripheral Edema and Ascites Ascites: - - Intraperitoneal accumulation of watery fluid containing small amounts of protein Ascites: - - Intraperitoneal accumulation of watery fluid containing small amounts of protein

35. Complications Peripheral Edema and Ascites Factors involved in the pathogenesis of ascites: - -Hypoalbuminemia - -  Levels of aldosterone - -  Portal hypertension Factors involved in the pathogenesis of ascites: - -Hypoalbuminemia - -  Levels of aldosterone - -  Portal hypertension

36. Complications Hepatic Encephalopathy Liver damage causes blood to enter systemic circulation without liver detoxification

37. Complications Hepatic Encephalopathy Main pathogenic toxin is NH 3 although other etiological factors have been identified Frequently a terminal complication Main pathogenic toxin is NH 3 although other etiological factors have been identified Frequently a terminal complication

38. Complications Fetor Hepaticus Musty, sweetish odor detected on the patient’s breath From accumulation of digested by- products Musty, sweetish odor detected on the patient’s breath From accumulation of digested by- products

39. Development of Ascites Fig. 42-6

40. Diagnostic Studies Liver function tests Liver biopsy Liver scan Liver ultrasound Liver function tests Liver biopsy Liver scan Liver ultrasound

41. Diagnostic Studies Esophagogastroduodenoscopy Prothrombin time Testing of stool for occult blood Esophagogastroduodenoscopy Prothrombin time Testing of stool for occult blood

42. Collaborative Care Rest Avoidance of alcohol and anticoagulants Management of ascites Rest Avoidance of alcohol and anticoagulants Management of ascites

43. Collaborative Care Prevention and management of esophageal variceal bleeding Management of encephalopathy Prevention and management of esophageal variceal bleeding Management of encephalopathy

44. Collaborative Care Ascites High carbohydrate, low protein, low Na+ diet Diuretics Paracentesis High carbohydrate, low protein, low Na+ diet Diuretics Paracentesis

45. Collaborative Care Ascites Peritoneovenous shunt –Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava Peritoneovenous shunt –Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

46. Peritoneovenous Shunt Fig. 42-8

47. Collaborative Care Esophageal Varices Avoid alcohol, aspirin, and irritating foods If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin) Avoid alcohol, aspirin, and irritating foods If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)

48. Collaborative Care Esophageal Varices Endoscopic sclerotherapy or ligation Balloon tamponade Surgical shunting procedures (e.g., portacaval shunt, TIPS) Endoscopic sclerotherapy or ligation Balloon tamponade Surgical shunting procedures (e.g., portacaval shunt, TIPS)

49. Sengstaken-Blakemore Tube Fig. 42-9

50. Portosystemic Shunts Fig. 42-11

51. Collaborative Care Hepatic Encephalopathy Goal: reduce NH 3 formation –Protein restriction (0-40g/day) –Sterilization of GI tract with antibiotics (e.g., neomycin) –lactulose (Cephulac) – traps NH 3 in gut –levodopa Goal: reduce NH 3 formation –Protein restriction (0-40g/day) –Sterilization of GI tract with antibiotics (e.g., neomycin) –lactulose (Cephulac) – traps NH 3 in gut –levodopa

52. Drug Therapy There is no specific drug therapy for cirrhosis Drugs are used to treat symptoms and complications of advanced liver disease There is no specific drug therapy for cirrhosis Drugs are used to treat symptoms and complications of advanced liver disease

53. Nutritional Therapy Diet for patient without complications: –High in calories –  CHO –Moderate to low fat –Amount of protein varies with degree of liver damage Diet for patient without complications: –High in calories –  CHO –Moderate to low fat –Amount of protein varies with degree of liver damage

54. Nutritional Therapy Patient with hepatic encephalopathy –Very low to no-protein diet Low sodium diet for patient with ascites and edema Patient with hepatic encephalopathy –Very low to no-protein diet Low sodium diet for patient with ascites and edema

55. Nursing Management Nursing Assessment Past health history Medications Chronic alcoholism Weight loss Past health history Medications Chronic alcoholism Weight loss

56. Nursing Management Nursing Diagnoses Imbalanced nutrition: less than body requirements Impaired skin integrity Ineffective breathing pattern Risk for injury Imbalanced nutrition: less than body requirements Impaired skin integrity Ineffective breathing pattern Risk for injury

57. Nursing Management Planning Overall goals: –Relief of discomfort –Minimal to no complications –Return to as normal a lifestyle as possible Overall goals: –Relief of discomfort –Minimal to no complications –Return to as normal a lifestyle as possible

58. Nursing Management Nursing Implementation Health Promotion –Treat alcoholism –Identify hepatitis early and treat –Identify biliary disease early and treat Health Promotion –Treat alcoholism –Identify hepatitis early and treat –Identify biliary disease early and treat

59. Nursing Management Nursing Implementation Acute Intervention –Rest –Edema and ascites –Paracentesis –Skin care –Dyspnea –Nutrition Acute Intervention –Rest –Edema and ascites –Paracentesis –Skin care –Dyspnea –Nutrition

60. Nursing Management Nursing Implementation Acute Intervention –Bleeding problems –Balloon tamponade –Altered body image –Hepatic encephalopathy Acute Intervention –Bleeding problems –Balloon tamponade –Altered body image –Hepatic encephalopathy

61. Nursing Management Nursing Implementation Ambulatory and Home Care –Symptoms of complications –When to seek medical attention –Remission maintenance –Abstinence from alcohol Ambulatory and Home Care –Symptoms of complications –When to seek medical attention –Remission maintenance –Abstinence from alcohol

62. Nursing Management Evaluation Maintenance of normal body weight Maintenance of skin integrity Effective breathing pattern No injury No signs of infection Maintenance of normal body weight Maintenance of skin integrity Effective breathing pattern No injury No signs of infection