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Cirrhosis by: Ashley Anderton, RN, BSN

Cirrhosis by: Ashley Anderton, RN, BSN. From the notes of: John Nation, RN, MSN Charlene Morris, RN, MSN Kelle Howard, MSN. RN, CNE. Cirrhosis Facts:. Progressive , leads to liver failure Insidious, prolonged course 9th leading cause of death in U.S. Twice as common in men

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Cirrhosis by: Ashley Anderton, RN, BSN

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  1. Cirrhosisby: Ashley Anderton, RN, BSN From the notes of:John Nation, RN, MSN Charlene Morris, RN, MSN Kelle Howard, MSN. RN, CNE

  2. Cirrhosis Facts: Progressive, leads to liver failure Insidious, prolonged course 9th leading cause of death in U.S. Twice as common in men Highest incidence between ages 40 and 60.

  3. What is Cirrhosis? Extensive destruction of liver cells Cells attempt to regenerate Regenerative process is disorganized Functional liver tissue is destroyed and scarring of liver occurs Overgrowth of fibrous connective tissue, distorting liver structure; obstructing blood flow

  4. Four Types of Cirrhosis: Alcoholic formerly called ________ Post-necrotic Biliary/obstructive Cardiac

  5. Alcoholic cirrhosis: Usually associated with alcohol abuse Most common cause of cirrhosis Causes metabolic changes in liver fat accumulates in liver (fatty liver) Fatty liver potentially reversible If alcohol abuse continues, widespread liver scar formation occurs

  6. Post Necrotic cirrhosis: Complication of: viral infections toxicity autoimmune hepatitis 20% of patient’s with chronic hepatitis C will develop cirrhosis Broad bands of scar tissue form within the liver

  7. Biliary cirrhosis: Associated with chronic biliary obstruction and/or infection Primary sclerosing cholangitis? Diffuse fibrosis of liver Jaundice is main feature www.humanillnesses.com

  8. Cardiaccirrhosis: Develops from long-standing right sided heart failure Results in patients with cor-pulmonale, constrictive pericarditis, and tricuspid insufficiency

  9. Diagnostic Studies: • Enzyme levels (AST, ALT) • initially elevated due to release from damaged liver cells • In end-stage liver disease • AST & ALT may be normal • Decrease: • total protein • albumin • Increase: • serum bilirubin • globulin levels • Prothrombin time prolonged

  10. Early Signs of cirrhosis: • Nausea and vomiting • Anorexia • Diarrhea or constipation • Pain • Fever • Weight loss

  11. Later Manifestations: Jaundice Skin Lesions/Spider angiomas Palmer erythema Thrombocytopenia, Leukopenia, Anemia Coagulation disorders Endocrine disturbance Peripheral neuropathy & peripheral edema

  12. Jaundice • Results from functional derangement of liver cells, compression of bile ducts • Liver’s decreased ability to excrete _________ • + Biliary obstruction, obstructive jaundice may occur accompanied by pruritus (accumulation of bile salts)

  13. Skin Lesions • WHY? • Dilated blood vessels (spider angiomas) • Palmarerythema

  14. Hematologic Problems • Thrombocytopenia • Leukopenia • Anemia • Vitamin K deficiency www.elements4health.com

  15. Endocrine Problems: • Inactivation of adrenocortical hormones • Men • Women • Hyperaldosteronism

  16. Peripheral Neuropathy & Peripheral Edema • Neuropathies due to: • Results in mixed nervous symptoms • Sensory symptoms are most common • Edema due to: http://www.jhu.edu

  17. Complications: • Portal Hypertension • Esophageal & Gastric Varices • Peripheral Edema & Ascites • Hepatic Encephalopathy

  18. Complications: Portal Hypertension • Compression and destruction of portal & hepatic veins • Increased venous pressure in portal circulation • Characterized by: • Collateral circulation develops

  19. Complications: Esophageal & Gastric Varices: • Esophageal: • Complex of twisting veins at lower end of esophagus • enlarged & swollen • Gastric- • upper portion of stomach • may occur alone or in combination with esophageal • Tolerate high pressure poorly, bleeding easily with distention • Rupture in response to irritation • Most life threatening complication!!

  20. Treatment for Varices: • Stop bleeding, manage airway, prevent aspiration of blood!! • Drug Therapy: • Propranolol, Sandostatin, Vasopressin, NTG • Band ligation of varices • Endoscopic sclerotherapy • thromboses and obliterates distended veins • Balloon tamponade-mechanical compresson of varices • Sengstaken-Blakesmore • Avoid: • alcohol & irritating foods • What common drugs should be avoided?

  21. Sengstaken-Blakesmore www. medical-dictionary.com

  22. Sengstaken-Blakemore Tube Three Lumens: • Esophageal balloon inflation • Gastric balloon inflation • Gastric aspiration

  23. Acute Bleed Supportive Measures: • FFP, PRBC’s, Vitamin K • Antibiotics • Protonix, Zantac • Propanolol • Prevent factors that may increase intra-abdominal pressure • Higher incidence of recurrent bleeds, so continued therapy is necessary!!

  24. Shunting Procedures: • Used more after 2nd major bleeding episode • TIPS • shunt is placed between systemic and portal venous systems • redirect’s portal blood flow • reduces portal venous pressure • decompresses varices • contraindicated in patient’s with hepatic encephalopathy

  25. TIPSTransjugular intrahepatic portosystemic shunt

  26. Complications: Ascites & Peripheral Edema • Results from impaired liver synthesis of albumin = hypoalbuminemia • Occurs as ankle and presacral edema • Ascites • accumulation of serous fluid in periotoneal or abdominal cavity • Hyperaldosteronism

  27. Four Factors Lead to Ascites Hypoproteinemia Increased Na+ & H2Oretention Increased capillary permeability Portal Hypertension

  28. www.patient.co.uk

  29. Nursing Management of ASCITES: Assess for respiratory distress Fowler’s position helps ease work of breathing Daily weights Measure abdominal girth Accurate I&O

  30. Medical Management of Ascites: • Na+ and Fluid restriction • Albumin • Diuretic therapy: • Aldactone, HCTZ, Lasix • Paracentesis • needle puncture of abdominal cavity to remove ascitic fluid- temporary • have patient void before procedure

  31. Management of Ascites: • Peritoneovenous Shunt • surgical procedure • provides continuous reinfusion of ascitic fluid into venous system • Not 1st line therapy due to high number of complications • Does not improve survival rates

  32. Hepatic Encephalopathy: • Terminal complication of liver disease • Disorder of protein metabolism and excretion • Ammonia • enters the systemic circulation without liver detoxification • crosses blood-brain barrier, causing neurologic toxic manifestations • Four stages of manifestations http://chemistry.about.com

  33. Where does ammonia come from? A by-product of protein metabolism Protein and amino acids are broken down by bacteria in GI tract, producing ammonia. Liver converts this to urea which is eliminated in the urine

  34. Hepatic Encephalopathy Stages0-1st Insomnia Personality changes Disturbances of awareness Forgetfulness, irritability, & confusion Trouble writing http://lukeromyn.com/blog

  35. Hepatic Encephalopathy Stages2nd & 3rd Lethargy, drowsiness Inappropriate speech Slurred speech Disorientation Asterixis flapping tremors Hiccups Hyperactive reflexes Violent behavior Slow, deep respirations Fetor hepaticus musty sweet smell to breath

  36. Hepatic Encephalopathy Stages4th + Babinski Possible seizures Swelling of brain tissue

  37. Treatment Hepatic Encephalopathy • Reduce ammonia formation • Lactulose • Control GI bleeding • Decreasing protein in intestine • Neomycin • Electrolyte replacement • Possible liver transplant • (depends on a number of factors)

  38. Hepatorenal Syndrome: • Serious complication • Functional renal failure with advancing azotemia, oliguria, and ascites • Portal hypertension + liver decompensation = decreased arterial blood volume & renal vasoconstriction • May be reversed by liver transplantation

  39. Nutritional Therapy: • High calorie/High Carb diet • Low protein diet • if Hepatic Encephalopathy present • Parenteral nutrition of tube feedings may be required • Low-sodium diet • if ascites and edema • Dietary education on reading labels at home www.reneerogers.com/nutrition

  40. Overall Goals: • Relief of discomfort • Minimal to no complications • (ascites, varices, hepatic encephalopathy) • Return to normal as possible lifestyle http://www.fontana.org/index

  41. Liver Dialysis Bridge to transplant Dialyze 6 hours at a time

  42. Donors: Live donor liver transplants are an excellent option. Liver regenerates to appropriate size for their individual bodies. Survival rates increase / shorter wait time The donor - a blood relative, spouse, or friend, will have extensive medical and psychological evaluations to ensure the lowest possible risk.

  43. Liver Transplantation • Blood type and body size are critical factors in determining who is an appropriate donor. • Potential donors evaluated for: • liver disease, alcohol or drug abuse, cancer, or infection. • hepatitis, AIDS, and other infections. • matched according to blood type and body size. • Age, race, and sex are not considered. • Cadaver donor have to wait

  44. http://www.murketing.com/journal

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