Liver cirrhosis

Nursing Management of patient with Liver cirrhosis

1. PARUL INSTITUTE OF NURSING Presented by : Nikhil Vaishnav M.Sc. Nursing LIVER CIRRHOSIS

2. INTRODCUTION

3. DEFINITION

4. Cirrhosis is a consequence of chronic liver disease, characterised by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules leading to loss of liver function.

5. INCIDENCE

6. CLASSIFICATION

7. Laennec’s cirrhosis, micronodular, portal cirrhosis. Men are more likely to have alcoholic cirrhosis. Fibrosis occurs mainly around central veins and portal areas. It is associated with chronic alcoholic abuse. Small nodules form as result of some offending agent. ALCOHOLIC CIRRHOSIS

8. Macronodular cirrhosis, toxin-induced cirrhosis. Most common worldwide form. Broad bands of scar tissue. Caused by postacute viral B, C hepatitis, Post intoxication with industrial chemicals. More common in women. POSTNECROTIC CIRRHOSIS

9. BILIARY CIRRHOSIS

10. CARDIAC CIRRHOSIS

11. CAUSES

12. CHRONIC ALCOHOLIC ABUSE

13. CHRONIC VIRAL HEPATITIS

14. NON-ALCOHOLIC FATTY LIVER DISEASE

15. Primary biliary cirrhosis Primary Sclerosing Cholangitis Biliary atresia Cystic fibrosis Hemochromatosis Wilson’s disease Budd cherry syndrome. OTHER CAUSES

16. Galactosemia or glycogen storage disease Autoimmune hepatitis Medication such as methotrexate, acetaminophen. Alagille syndrome. Infection such as syphilis Amyloidosis

17. STAGES OF LIVER DAMAGE

18. CLINICAL MENIFESTATIONS

19. SYSTEMIC CLINICAL MENIFESTATIONS OF LIVER CIRRHOSIS

20. NEUROLOGIC

21. ASTERIXIS

22. Anorexia Dyspepsia Nausea, vomiting Change in bowel habits Dull abdominal pain GASTROINTESTINAL

23. Gastritis Hematemesis Fetor hepaticus Esophageal and gastric verices. Hemorrhoidal verices Contd.

24. Amenorrhea( Younger women) Testicular atrophy Gynecomastia Impotence with loss of libido Loss of axillary and pubic hair Vaginal bleeding( Older women) REPRODUCTIVE

25. Jaundice Spider angioma Palmar erythema Purpura Petechiae Caput medusae INTEGUMENTARY

26. Blood spots/ skin hemorrhage Purple spots due to low platelets. PURPURA

27. JAUNDICE

28. Also known as spider nevus. Common in people with alcoholic cirrhosis. It is the enlarged blood vessel in skin due to high estrogen level. SPIDER ANGIOMA

29. Also called liver palms . Reddening of both of the palms due to excess estrogen. PALMAR ERTHEMA

30. These are large visible distended, engorged paraumbilacal veins due to severe portal hypertension. CAPUT MADUSAE

31. Hypokalemia Hyponatremia Hypoalbuminemia METABOLIC

32. Anemia Thrombocytopenia Leukopenia Coagulation disorders Splenomegaly HEMATOLOGIC

33. Fluid retention Peripheral edema Ascites CARDIOVASCULAR

34. History collection Physical examination Elevated liver enzymes such as AST, ALT, GGT, ALP. Increased serum bilirubin. Liver ultrasound to assess the severity of cirrhosis. Liver biopsy to identify liver cell changes & alterations in the lobular structure. Prolonged prothrombin time

35. Complete blood count. Serum electrolytes. Esophagogastroduodenoscopy also known as upper endoscopy. CT scan Decreased cholesterol level due to abnormal fat metabolism. Decreased albumin. Increased globulin. Paracentesis to examine ascitic fluid for cell, protein, bacterial counts. PTC

36. Portal vein delivers blood from the intestine to the liver. Due to cirrhosis there is increased resistance or obstruction of blood flow through the portal venous system into the liver. Normal portal venous blood pressure is 5 to 10 mm Hg. High portal pressure causes collateral vessels to develop in lower esophagus , the anterior abdominal wall, the rectum, parietal peritoneum. PORTAL HYPERTENSION

37. Portal hypertension is mainly characterized by Splenomegaly, Large collateral veins, ascites. Collateral circulation develops to reduce the high portal pressure. s/s are Ascites, Splenomegaly, hemorrhoids, gastric and esophageal varices , superficial abdominal veins.

38. Esophageal varices are complex of tortuous veins at the lower end of esophagus, which are enlarged and swollen as a result of portal hypertension. Gastric varices are located in the upper portion of the stomach. Large varices are more likely to bleed . Esophageal varices are responsible for 80 % of variceal hemorrhage. OESOPHAGEAL & GASTRIC VARICES

39. Bleeding of varices occurs due to alcohol ingestion, erosion by gastric juices, Increased abdominal pressure by coughing, sneezing, straining at stool, nausea, vomiting, lifting heavy objects. The patient may have melena and Hematemesis. The massive hemorrhage is a medical emergency.

40. ASCITES & PERIPHERAL EDEMA

41. HEPATIC ENCEPHALOPATHY

42. PATHOPHYSIOLOGY

43. CLINICAL MENIFESTATIONS

44. SPONTANEOUS BACTERIAL PERITONITIS

45. HEPATORENAL SYNDROME

46. HEPATORENAL SYNDROME

47. HEPATOCELLULAR CARCINOMA

48. MANAGEMENT

49. TREATMENT OF ASCITES

50. Paracentesis: It may be performed to remove ascitic fluid or to test the fluid for infection ( spontaneous bacterial peritonitis) . It is done for the patient with impaired respiration or abdominal pain caused by severe ascites. It is a temporary measure. Contd.

51. Peritoneovenous shunt is a surgical procedure that reinfuse ascitic fluid into the venous system . Because of high complications it is not used now.

52. TREATMENT OF OSOPHAGEAL & GASTRIC VARICES

53. ENDOSCOPIC BAND LIGATION: Endoscopic variceal ligation or banding is performed by placing a small rubber band around the base of the varix(enlarged vein).

54. SCLEROTHERAPY: It involves injection of a sclerosant solution into the varices through an injection needle that is placed through the endoscope.

55. BALLOON TAMPONADE

56. SENGSTAKEN – BLAKEMORE TUBE

57. MINNESOTA TUBE

58. SUPPORATIVE MEASURES

59. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT(TIPS)

60. TIPS

61. SURGICAL SHUNTING(PORTOSYSTEMIC SHUNTS)

62. PORTACAVAL SHUNT

63. DISTAL SPLENORENAL SHUNT

64. TREATMENT OF HEPATIC ENCEPHALOPATHY

65. It is final resort for the treatment of Liver cirrhosis. LIVER TRANSPLANATION

66. High calorie(3000 cal/day) with high carbohydrate , moderate to low levels of fat. Protein restriction is done in patients with severe hepatic encephalopathy only. BCAA is recommended to treat protein calorie malnutrition. The patients with ascites and edema is on a low sodium diet. Foods that are high in sodium should be avoided. NUTRITIONAL THERAPY

67. Subjective data includes past health history , medications. Assess the client closely for the presence of early menifestations such as Hepatomegaly. Carefully check the laboratory data for any indication of cirrhosis. As the disease progresses, complications such as ascites, portal hypertension or hepatic encephalopathy should be observed. Assess the client and family members for their knowledge of important aspects of self care. NURSING ASSESSMENT

68. Monitor the client for bleeding gums, Purpura melena, hematuria, Hematemesis. Check vital signs for signs of shock. Monitor urine output. Protect the client from physical injury from falls or abrasions. Instruct the client to avoid vigorous nose blowing and straining with bowel movements. Stool softeners are given to prevent straining with rupture of varices. INTERVENTIONS

69. The diet should provide ample protein to rebuild tissue but not enough protein to precipitate hepatic encephalopathy. The diet should supply sufficient carbohydrates to maintain weight. If client has ascites, edema sodium should be restricted. Small, frequent meal is easier to anorexia. INTERVENTIONS

70. Long term planning should include counseling the client to rest frequently and to avoid unnecessary fatigue. INTERVENTION

71. All known hepatotoxins including alcohol are removed from the therapeutic regimens. Avoid the administration of sedatives and opoids.

72. Monitor for menifestations of infection and administer antibiotics as needed. Antibiotics may be required to control instestinal flora that aggravate encephalopathy.