Text of Cirrhosis by: Ashley Anderton, RN, BSN From the notes of: John Nation, RN, MSN Charlene Morris, RN,...
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Cirrhosis by: Ashley Anderton, RN, BSN From the notes of: John Nation, RN, MSN Charlene Morris, RN, MSN Kelle Howard, MSN. RN, CNE
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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.
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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
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Four Types of Cirrhosis: Alcoholic formerly called ________ Post-necrotic Biliary/obstructive Cardiac
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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
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Post Necrotic cirrhosis: Complication of: viral infections toxicity autoimmune hepatitis 20% of patients with chronic hepatitis C will develop cirrhosis Broad bands of scar tissue form within the liver
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Biliary cirrhosis: Associated with chronic biliary obstruction and/or infection Primary sclerosing cholangitis? Diffuse fibrosis of liver Jaundice is main feature www.humanillnesses.com
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Cardiac cirrhosis: Develops from long-standing right sided heart failure Results in patients with cor-pulmonale, constrictive pericarditis, and tricuspid insufficiency
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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
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Early Signs of cirrhosis: Nausea and vomiting Anorexia Diarrhea or constipation Pain Fever Weight loss
Jaundice Results from functional derangement of liver cells, compression of bile ducts Livers decreased ability to excrete _________ + Biliary obstruction, obstructive jaundice may occur accompanied by pruritus (accumulation of bile salts)
Hematologic Problems Thrombocytopenia Leukopenia Anemia Vitamin K deficiency www.elements4health.com
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Endocrine Problems: Inactivation of adrenocortical hormones Men Women Hyperaldosteronism
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Peripheral Neuropathy & Peripheral Edema Neuropathies due to: Results in mixed nervous symptoms Sensory symptoms are most common Edema due to: http://www.jhu.edu
Complications: Portal Hypertension Compression and destruction of portal & hepatic veins Increased venous pressure in portal circulation Characterized by: Collateral circulation develops
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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!!
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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?
Acute Bleed Supportive Measures: FFP, PRBCs, Vitamin K Antibiotics Protonix, Zantac Propanolol Prevent factors that may increase intra-abdominal pressure Higher incidence of recurrent bleeds, so continued therapy is necessary !!
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Shunting Procedures: Used more after 2 nd major bleeding episode TIPS shunt is placed between systemic and portal venous systems redirects portal blood flow reduces portal venous pressure decompresses varices contraindicated in patients with hepatic encephalopathy
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
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Increased capillary permeability Increased Na + & H 2 O retention Portal Hypertension Hypoproteinemia Four Factors Lead to Ascites
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www.patient.co.uk
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Nursing Management of ASCITES: Assess for respiratory distress Fowlers position helps ease work of breathing Daily weights Measure abdominal girth Accurate I&O
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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
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Management of Ascites: Peritoneovenous Shunt surgical procedure provides continuous reinfusion of ascitic fluid into venous system Not 1 st line therapy due to high number of complications Does not improve survival rates
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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
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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
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Hepatic Encephalopathy Stages 0-1 st Insomnia Personality changes Disturbances of awareness Forgetfulness, irritability, & confusion Trouble writing http://lukeromyn.com/blog
Hepatic Encephalopathy Stages 4 th + Babinski Possible seizures Swelling of brain tissue
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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)
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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
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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
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Overall Goals: Relief of discomfort Minimal to no complications (ascites, varices, hepatic encephalopathy) Return to normal as possible lifestyle http://www.fontana.org/index
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Liver Dialysis Bridge to transplant Dialyze 6 hours at a time
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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.
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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,
