Cirrhosis of liver - Seminar. pptx

The Seminar consist of Definition
Epidemiology
Causes
Pathophysiology
Clinical manifestations
Diagnostic measures
Management
Complications
Nursing Management

1. CIRRHOSIS Shashi Prakash M.Sc. Nursing, II Year CON, ILBS

2. CONTENT Definition Epidemiology Causes Pathophysiology Clinical manifestations Diagnostic measures Management Complications Nursing Management

3. INTRODUCTION The word "cirrhosis" is a neologism derived from Greek kirrhós meaning "yellowish, tawny" and the suffix - osis , i.e. "condition" in medical terminology.

4. INTRODUCTION End-stage Liver disease Chronic in nature Liver does not function properly due to long-term damage. Replacement of normal liver tissue by scar tissue.

5. INTRODUCTION The cost of cirrhosis in terms of human suffering, hospital costs, and lost productivity is high.

6. DEFINITION A chronic liver disease characterized by fibrotic changes and the formation of dense connective tissue within the liver, subsequent degenerative changes, and loss of functioning cells. A chronic progressive disease of the liver characterised by extensive degeneration and destruction of the liver cells.

7. EPIDEMIOLOGY Cirrhosis affected about 2.8 million people and resulted in 1.3 million deaths in 2015. Of these deaths, alcohol caused 3, 48, 000, hepatitis C caused 326,000, and hepatitis B caused 3, 71, 000. Cirrhosis is the 12 leading cause of death due to disease in the United States (NIH).

8. EPIDEMIOLOGY In the United States, more men die of cirrhosis than women. India Around 10 lakh clients of liver cirrhosis are newly diagnosed every year Liver disease may affect every one in 5 Indians. Liver disease is the tenth most common cause of death (WHO)

9. EPIDEMIOLOGY Established cirrhosis has a 10 year mortality of 34- 66 %. Largely dependent on the cause of the cirrhosis Alcoholic cirrhosis has a worse prognosis than primary biliary cholangitis and hepatitis.

10. CAUSES More than one cause is present in the same person. Globally, 57% of cirrhosis is attributable to either hepatitis B (30%) or hepatitis C (27%). Alcohol consumption is another major cause, accounting for about 20% of the cases.

11. CAUSES Alcoholism Chronic viral hepatitis Hepatitis B Hepatitis C Autoimmune hepatitis NASH

12. CAUSES Biliary cirrhosis Primary biliary cirrhosis Primary Sclerosing cholangitis Autoimmune cholangiopathy Cardiac cirrhosis Inherited metabolic liver disease

13. CAUSES Hemochromatosis Wilson’s disease Cystic fibrosis Cryptogenic cirrhosis

14. PATHOPHYSIOLOGY OF LIVER CIRRHOSIS Liver insult, Alcohol ingestion, Viral hepatitis, Exposure to toxins Liver necrosis Hepatocyte damage Liver inflammation Alterations in blood and lymph flow Decreased ADH and aldosterone detoxification Decreased androgen and estrogen detoxification Decreased metabolism of protein and carbohydrate Decreased vitamin K absorption Decreased bilirubin metabolism and biliary tree damage or obstruction

15. Oedema Palmar erythema, spider angiomas Ascites, Hypoglycaemia Bleeding tendencies Jaundice. Clay- colored stools, Dark urine Liver fibrosis and scarring Liver failure PATHOPHYSIOLOGY OF LIVER CIRRHOSIS

16. CLASSIFICATION Micronodular Macronodular Mixed

17. MICRONODULAR Alcohol Hemochromatosis Hepatic venous outflow obstruction Chronic biliary obstruction Jejunoileal bypass

18. MACRONODULAR Hepatitis B Hepatitis C Primary biliary cholangitis.

19. TYPES Alcoholic Cirrhosis Post-necrotic Cirrhosis Biliary Cirrhosis Cardiac Cirrhosis

20. ALCOHOLIC CIRRHOSIS Previously called Laennec’s cirrhosis (René Laennec) Also called Portal or nutritional cirrhosis. Alcoholic cirrhosis develops for 10-20% of individuals who drink heavily for a decade or more.

21. ALCOHOLIC CIRRHOSIS Ethanol alcohol dehydrogenase acetaldehyde Acetaldehyde acetaldehyde dehydrogenase acetate Increases intracellular accumulation of triglycerides by increasing fatty acid uptake and by reducing fatty acid oxidation and lipoprotein secretion.

22. Formation of protein-acetaldehyde adducts Interfere with specific enzyme activities, including microtubular formation and hepatic protein trafficking Hepatocyte damage Reactive oxygen species activate Kupffer species

23. Production of profibrogenic cytokines Perpetuate stellate cell activation Production of excess collagen, extracellular matrix

24. POST-NECROTIC CIRRHOSIS It is a complication of viral, toxic or idiopathic (autoimmune hepatitis). Broad bands of scar tissue forms within the liver. BILIARY CIRRHOSIS Biliary cirrhosis is associated with chronic biliary obstruction and infection. There is diffuse fibrosis of the liver with jaundice as a main feature.

25. CARDIAC CIRRHOSIS It results from long standing, severe right-sided heart failure in clients with cor-pulmonale , constrictive pericarditis, and tricuspid insufficiency.

26. CARDIAC CIRRHOSIS Elevated venous pressure transmitted via the inferior vena cava and hepatic veins to the sinusoids of the liver, which become dilated and engorged with blood. The liver becomes enlarged and swollen With long-term passive congestion and relative ischemia due to poor circulation, hepatocytes can become necrotic, leading to fibrosis.

27. PATHOPHYSIOLOGY

28. PATHOPHYSIOLOGY The progression rate from fibrosis to cirrhosis and the morphology of cirrhosis vary from person to person. Presumably, the reason for such variation is the extent of exposure to the injurious stimulus and the individual’s response. Hepatic fibrosis Regenerating liver cells

29. Hepatocyte injury and loss Growth regulator- cytokines Hepatic growth factors – epithelial growth factor, hepatocyte growth factor, transforming growth factor-alpha, tumor necrosis factor Hepatocellular hyperplasia and angiogenesis

30. Clinical picture of a client with liver dysfunction

31. CLINICAL MANIFESTATIONS Early manifestations Onset of cirrhosis is usually insidious. Occasionally there is abrupt onset of symptoms. GI disturbances are common.

32. EARLY MANIFESTATIONS Anorexia Dyspepsia Flatulence Nausea and vomiting Change in bowel habits (Diarrhoea and constipation)

33. EARLY MANIFESTATIONS Abdominal pain Fever Lassitude Slight weight loss Liver and spleen enlargement

34. LATER MANIFESTATIONS It may be severe and result from liver failure and its complications. Jaundice Skin lesions Spider angiomata and Palmer erythema

35. LATER MANIFESTATIONS Haemotological probems : Thrombocytopenia, leukopenia, anaemia, and coagulation disorders. Coagulation problems manifested by epistaxis, purpura , petechiae, easy bruising, gingival bleeding, and heavy menstrual bleeding. Peripheral neuropathy

36. LATER MANIFESTATIONS Endocrine problems Men: Gynecomastia , loss of axillary, pubic hair, testicular atrophy, impotence with loss of libido. Younger women: amenorrhoea Older women: vaginal bleeding Hyperaldosteronism causes sodium and water retention and potassium loss.

37. Compensated cirrhosis Decompensated cirrhosis Intermittent mild fever Vascular spiders Palmar erythema Unexplained epistaxis Ankle edema Vague morning indigestion Flatulent dyspepsia Abdominal pain Firm, enlarged liver Splenomegaly Ascites Jaundice Weakness, Muscle wasting Weight loss Continuous mild fever Purpura Spontaneous bruising Epistaxis Hypotension Sparse body hair Gonadal atrophy

38. DIAGNOSIS The gold standard for diagnosis of cirrhosis is a liver biopsy The best predictors of cirrhosis are ascites, platelet count <160,000/mm3, spider angiomata , and a Bonacini cirrhosis discriminant score greater than 7.

39. Bonacini score Score Platelet count x10 9 AST/ALT Ratio INR > 340 > 1.7 < 1.1 1 280 - 340 1.2 - 1.7 1.1 - 1.4 2 220 - 279 0.6 - 1.19 > 1.4 3 160 - 219 < 0.6 --- 4 100 - 159 ... ... 5 40 - 99 ... ... 6 < 40 ... ...

40. LABORTAORY FINDINGS Thrombocytopenia Aminotransferases Alkaline phosphatase - slightly elevated but less than 2–3 times the upper limit of normal. Gamma- glutamyltransferase - correlates with ALP levels. Typically much higher in chronic liver disease from alcohol.

41. LABORTAORY FINDINGS Bilirubin Albumin Prothrombin time Globulins- increased due to shunting of bacterial antigens away from the liver to lymphoid tissue. Leukopenia and neutropenia Coagulation defects

42. LABORATORY FINDINGS Fibro scan (>14 kPa) USG : Small, nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas. Other liver findings suggestive of cirrhosis are an enlarged caudate lobe, widening of the fissures and enlargement of the spleen.

43. Liver biopsy: Gold standard for Diagnosis of cirrhosis Sequential histological grading of inflammation and staging of fibrosis can assess risk of progression Microscopy The presence of regenerating nodules of hepatocytes Presence of fibrosis

44. LIVER BIOPSY Chronic hepatitis B : infiltration of the liver parenchyma with lymphocytes Cardiac cirrhosis : Erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins Primary biliary cholangitis : fibrosis around the bile duct, the presence of granulomas and pooling of bile

45. LIVER BIOPSY Alcoholic cirrhosis : infiltration of the liver with neutrophils Child- Pugh score Also known as Child- Turcotte -Pugh score or Child Criteria Devised in 1964 by Child and Turcotte , and modified in 1973 by Pugh and others

46. Child- Turcotte -Pugh Score Measure 1 point 2 points 3 points Total bilirubin, μmol/L (mg/dL) <34 (<2) 34- 50 (2–3) >50 (>3) Serum albumin, g/dL >3.5 2.8- 3.5 <2.8 Prothrombin time, prolongation (s) < 4.0 4.0- 6.0 > 6.0 INR <1.7 1.7–2.3 > 2.3 Ascites None Mild (or suppressed with medication) Moderate to severe (or refractory) Hepatic encephalopathy None Grade I–II Grade III–IV

47. Child- Pugh score Interpretation Points Class One-year survival Two-year survival 5–6 A 100% 85% 7–9 B 80% 60% 10–15 C 45% 35 %

48. COMPLICATIONS Portal hypertension Esophageal & gastric varices Peripheral edema Ascites Hepatic Encephalopathy Hepatorenal Syndrome

49. PORTAL HYPERTENSION Because of the structural changes in the liver from cirrhotic process, there is compression and destruction of the portal and hepatic veins and sinusoids. These changes cause obstruction to the normal flow of blood through the portal system, resulting in portal hypertension. It is defined as HVPG greater than or equal to 5 mm Hg and is considered to be clinically significant when HVPG exceeds 10 to 12 mm Hg.

50. Collateral circulation develops These collateral and systemic circulations communicate to develop varicosities such as esophageal, gastric, caput medusa and haemorrhoids

51. ESOPHGAEAL & GASTRIC VARICES These collateral vessels contain little elastic tissue and are quite fragile. They tolerate high pressure poorly resulting in distension and bleed easily.

52. PERIPHERAL EDEMA Edema results from decreased colloidal oncotic pressure from impaired liver synthesis of albumin and increased portacaval pressure from PHTN. Peripheral edema occurs as ankle and presacral edema.

53. ASCITES When blood pressure is elevated in the liver as occurs in cirrhosis, proteins move from the blood vessels via the large pores of the sinusoids (capillaries) into the lymph space. When the lymph system is unable to carry off the excess proteins and water, they leak through the liver capsule into the peritoneal cavity. The osmotic pressure of the proteins pulls additional fluid into the peritoneal cavity.

54. ASCITES Hypoalbuminemia causes decreased colloidal oncotic pressure. Damaged hepatocytes does not metabolise aldosterone. The increased level of aldosterone causes increased sodium reabsorption by the renal tubules and therfore additional water retention. Because of edema formation there is decreased intravascular volume and subsequently decreased renal flow and glomerular filteration .

55. HEPATORENAL SYNDROME Functional renal failure with advancing azometia , oliguria, and intractable ascites without structural abnormality of the kidneys

56. HRS Type 1 HRS is characterized by a progressive impairment in renal function and a significant reduction in creatinine clearance within 1–2 weeks of presentation. Type 2 HRS is characterized by a reduction in glomerular filtration rate with an elevation of serum creatinine level, but it is fairly stable and is associated with a better outcome than that of Type 1 HRS.

57. Portal Hypertension Splanchnic vasodilation Decreased effective circulatory volume Activation of renin-angiotensin-aldosterone system Renal sodium activity Renal vasoconstriction Ascites Hepatorenal Syndrome

58. COMPLICATIONS Malnutrition Abnormalities in coagulation Bone diseases Hematological Abnormalities

59. MANAGEMENT Stop the progression Manage complications Nutritional Therapy Treat cause

60. Ascites Sodium restriction Based on the degree of ascites. Initially sodium intake to 2g/day Severe ascites : sodium intake to 250-500 mg/day. Diuretic therapy : A high potency loop diuretic such as furosemide in combination with potassium sparing diuretic such as spironolactone. Paracentesis

61. Portosystemic shunt

62. Complications Thrombosis formation at the venous tip of the shunt Infection Shunt occlusion

63. Esophageal & gastric varices Avoid ingesting alcohol, aspirin, irritating foods, prompt treatment of upper respiratory infections and controlled cough Drug therapy ( Somatostatin analog octreotide, vasopressin, nitroglycerine , and beta adrenergic blockers such as propranolol) Endoscopic therapies include sclerotherapy , ligation of varices

64. Hepatic encephalopathy Lactulose Lactulose in the colon is split into lactic acid and acetic acid which decreases pH from 7 to 5. The acidic environment discourages bacterial growth. Also, it traps the ammonia in the gut and the laxative effect of the drug expels the ammonia from the colon. Antibiotics such as metronidazole, vancomycin , rifaximin to reduce the bacterial flora of the colon.

65. Drug Mechanism Vasopressin Hemostasis and control of bleeding in esophageal varices , constriction of splanchnic arterial bed. Propranolol Reduction of portal venous pressure, reduction of esophageal varices bleeding Vitamin K Correction of clotting abnormalities Histamine receptor blockers and proton pump inhibitors Decreases gastric acidity Diuretics Spironolactone Furosemide Blocks action of aldosterone, potassium sparing Acts on distal tubule and loop of Henle to prevent reabsorption of sodium and water Fat soluble vitamins , Thiamine, Zinc supplementations

66. DRUG THERAPY Acetylcysteine N- acetylcysteine (NAC) is a hepatoprotective agent that turns into the amino acid L-cysteine when ingested. In turn, L-cysteine helps produce glutathione (GSH) that helps produce the antioxidant glutathione, which plays a key role in protecting the liver from damage.

67. MANAGEMENT Nutritional Therapy Without complications: High in calories (3000 kcal/day) with high carbohydrate content and moderate to low fat levels. Hepatic encephalopathy: Protein restriction Ascites & edema: Low sodium diet

68. MANAGEMENT Alcoholic cirrhosis: High in protein, calorie Enteral formulas Liver Transplantation It is considered in patients with recurring hepatic encephalopathy and end-stage liver disease. It depends upon factors - cause of the cirrhosis and other systemic medical problems.

69. NURSING MANAGEMENT

70. Horta’s Conceptual Model

71. NURSING ASSESSMENT •Assess for presence of haemorrhage, hypovolemia and oliguria •Assess the client’s respiratory, renal and hemodynamic status. •Fluid and electrolyte imbalances, hypoglycaemia. •Manifestations of infections (fever, increased white blood cells). •Pain levels. •Mental status of the client.

72. NURSING MANAGEMENT Ineffective breathing pattern related to ascites and restriction of thoracic excursion secondary to ascites, abdominal distention, and fluid in the thoracic cavity. Chronic pain and discomfort related to enlarged tender liver and ascites

73. NURSING MANAGEMENT Haemorrhage related to bleeding tendency secondary to altered clotting factors and rupture of esophageal or gastric varices .

74. NURSING MANAGEMENT Fluid volume excess related to ascites and edema formation. Disturbed thought processes related to deterioration of liver function and increased serum ammonia level. Imbalanced nutrition: less than body requirements, related to abdominal distention, discomfort and anorexia.

75. NURSING MANAGEMENT Activity intolerance related to fatigue, lethargy, and malaise. High risk for injury related to altered clotting mechanisms and altered level of consciousness.

76. EXERCISES FOR LIVER CIRRHOTIC PATIENTS

77. DIETARY PATTERN IN LIVER CIRRHOSIS Low-sodium diet Adequate protein intake to prevent muscle wasting. Omega-6 fatty acids should be avoided as it can lead to toxic lipid metabolites. Fluid-restricted diet. A nighttime snack of approximately 700 calories and approximately 25 grams of protein Vitamin A, D, Zinc and Magnesium supplementation. Branched-chain amino acids (BCAAs) Oral and enteral nutritional supplementation Probiotic treatment Coffee consumption

78. HEALTH EDUCATION Cirrhosis of the liver is a life-threatening chronic illness, which is ultimately terminal without transplantation. However, the management of some cirrhosis cases may be improved with diet, thorough compliance with prescribed medications, and abstinence from alcohol.

79. SUMMARY

80. CONCLUSION Cirrhosis is defined as the histological development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury, that leads to portal hypertension and end stage liver disease. Alcoholic liver disease and hepatitis C are the most common causes in the Western world, while hepatitis B prevails in most parts of Asia and sub-Saharan Africa. The ultimate therapy for cirrhosis and end stage liver disease is liver transplantation.

81. BIBLIOGRAPHY Bacon, B. R. (2018). Cirrhosis and Its Complications. Longo, D.L., Kasper, D.L., Jameson, J.L., Fauci , S. A., Hauser, S.L., Fishman, A.R., & Loscalzo , J (Eds.), Harrison Principals of Internal Medicine (pp. 2592- 2602). New Delhi: MacGraw Hill. Cirrhosis. 2019. Retrieved May 22, 2019 from https://en.wikipedia.org/wiki/Cirrhosis.   Schuppan , D., & Afdhal , N. H. (2008). Liver Cirrhosis. Lancet, 371 (9615), 838–851. doi : 10.1016/S0140-6736(08)60383-9

82. BIBLIOGRAPHY Smeltzer , C. S., Bare, G. B., Hinkle, L. J., & Cheever, H. K. (2011). Brunner & Suddarth Textbook of Medical-Surgical Nursing (11 th ed.) Nehru Place, New Delhi: Wolters Kluwer. Black, J., M.(2010). Medical Surgical nursing. Eighth Edition. Published by Elsevier, a division of Reed Elsevier India Private Limited: 1147 -69. Norton, C.(2008). Gastrointestinal Nursing. First Edition. Published by Oxford University Press Inc. New York: 401-6 www.pubmed.ncbi

83. Thankyou