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,
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