Ppt on Liver cirrhosis, management and its prevention.pptx

this document content about liver cirrhosis and its management. It begins with introduction of liver cirrhosis, definition, incidence, causes, etiology, classification, pathophysiology, stages of liver damage, clinical manifestations, diagnostic evaluation, medical management, surgical management, nursing management and prevention of liver cirrhosis.

1. Liver cirrhosis By: Maishnam Sanathoi Devi

2. New Employee Orientation Getting to know your new assignment Familiarizing yourself with your new environment Meeting new colleagues

3. INTRODUCTION It is a chronic disease in which there has been diffuse destruction and fibrotic regeneration of hepatic cells.

4. As necrotic tissue is replaced by fibrotic tissue, normal liver structure and vasculature is altered, impairing blood and lymph flow. It result in hepatic insufficiency and portal hypertension. INCIDENCE Cirrhosis is the 8 th leading cause of death in United states and 12 th leading cause of deaths in world by 2020. Around 20% of patients with chronic HCV and 10-20 % of patients with chronic HBV develop cirrhosis. Men are doubly affected than women. Highest incidence occurs in age 40-60 years.

5. DEFINITION Cirrhosis of liver is a chronic progressive disease characterized by degeneration and destruction of normal liver tissue and replacement with fibrous tissue and regenerative nodules leading to loss of normal liver function . It is a chronic, progressive disease characterized by widespread fibrosis (scarring) and nodule formation .

6. Etiology and risk factors Chronic viral infections of the liver (hepatitis types B & C) Fatty liver associated with obesity and diabetes Alcohol abuse, Biliary cirrhosis , Cystic fibrosis Hemochromatosis (iron overload) Wilson’s disease (copper diposition ) Budd cherry syndrome (occlusion of hepatic vein ) Galactosemia or glycogen storage disease Autoimmune hepatitis Medication such as methotrexate, acetaminophen Infection such as syphilis Amyloidosis (deposition of amyloid protein)

7. Pathophysiology Technology Procedure Policies Benefits

8. Excessive alcohol ingestion Cell protein damage Inflammatory cell infiltration Cirrhosis Destructive metabolites hepatomegaly Fat accumulation in hepatocytes Exaggerated detoxification activity

9. New Work

10. New Work

11. CLINICAL MANIFESTATIONS Early manifestation: Onset is gradual. Early symptom is fatigue. Later manifestations: Later symptom may be severe and result from liver failure and portal hypertension Jaundice, ascites, peripheral edema develop gradually. Other late symptoms include skin lesions, disturbances, peripheral neuropathies etc.

12. Systemic clinical manifestation

13. History collection Physical examination Liver function test. Elevated enzymes such as AST, ALT, GGT, ALP, increased serum bilirubin Liver ultrasound to assess the severity of cirrhosis and reveals irregular nodular liver. Liver biopsy to identify liver cell changes & alteration in the lobular structure Complete blood count reveals anemia, leukopenia and thrombocytopenia. Diagnostic Evaluation

14. Serum electrolytes studies show hypernatremia and hypokalemia. Esophagogastroduodenoscopy also known as upper endoscopy. CT scan, MRI and radioisotope liver scan provide information about liver size and hepatic blood flow and obstruction. Stool test for occult blood Paracentesis to examine ascitic fluid for cell, protein, bacterial counts. PTC (Percutaneous transhepatic cholangiography)

15. MANAGEMENT Rest and good diet Correction of nutritional deficiencies with vitamins and nutritional supplements and a high-calorie and moderate to high protein diet. Treatment for underlying cause. Prevention of further liver damage by avoiding use of alcohol, paracetamol , IV drug abuse and other hepatotoxic drugs. Provide symptomatic treatment

16. Treatment of ascites and fluid and electrolyte imbalances : Restrict sodium and water intake depending on amount of fluid retention. Bed rest to aid in diuresis Diuretic therapy, frequently with spironolactone ( Aldactone ), a potassium-sparing diuretic that inhibits the action of aldosterone on the kidneys.

17. Furosemide ( lasix ), a loop diuretic, may also be used in conjunction with spironolactone to help balance potassium depletion Abdominal paracentesis to remove fluid and relieve symptoms Ascitic fluid may be ultrafiltrated and reinfused through a central venous access Administration of albumin to maintain osmotic pressure

18. Transjugular intrahepatic portosystemic shunt (TIPS)

19. Prevention of bleeding and hemorrhage – avoid ingesting alcohol, aspirin or irritating food. Management of bleeding varices – a combination of drug therapy and endoscopic therapy is more effective. Drug therapy – vasopressin , beta blockers Endoscopic therapy – it comprises of sclerotherapy , ligation of varices and shunt therapy

20. Balloon temponade – it controls bleeding by mechanical compression of the varices . Sengstaken -Blakemore tube is used for this purpose. Supportive therapy during an acute hemorrhage include administration of fresh frozen plasma, packed RBCs, vitamin K, histamine ( H 2 ) receptors blockers e.g. renitidine , proton pump inhibitors; lactulose and neomycin to prevent hepatic encephalopathy from break down of blood and release ammonia in the intestine. Liver transplantation

21. COMPLICATIONS Portal hypertension Swelling (edema) in your legs, ankles or feet Ascites Splenomegaly Hepatopulmonary syndrome Hepatorenal syndrome 2 Hyponatremia and water retension Bleeding esophageal varices 4 Coagulopathies Spontaneous bacterial Peritonitis Hepatic encephalopathy Hypersplenism Infections Malnutrition Liver cancer Liver failure gallstone

22. NURSING MANAGEMENT Obtain history of precipitation factors, such as alcohol abuse, hepatitis, or biliary disease. Assess mental status through interview and interaction with the patient. Perform abdominal examination, assessing for ascites. Observe for bleeding. Assess daily weight and abdominal girth measurements.

23. NURSING DIAGNOSIS Activity intolerance related to fatique , general debility, muscle weakness, abdominal pain and discomfort secondary to ascites as evidenced by patients verbal complain about weakness, tachycardia and tachypnea on exertion. Imbalanced nutrition less than body requirements related to dyspepsia, abdominal distention , reduced gastric motility as evidenced by lack of interest in food. Impaired skin integrity related to edema , ascites and jaundice as evidenced by complaints of itching, evidence of scratch mark on skin.

24. Ineffective breathing pattern related to intra-abdominal fluid collection, decreased lung expansion, accumulated secretions. Fluid volume excess related to compromised regulatory mechanism or excess sodium and fluid intake. Risk of injury and bleeding related to altered clotting mechanisms as evidenced by complaints of gum bleeding, epistaxis. Risk for acute confusion related to alcohol abuse or liver encephalopathy.