cirrhosis by: ashley anderton, rn, bsn
DESCRIPTION
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 - PowerPoint PPT PresentationTRANSCRIPT
Cirrhosisby: Ashley Anderton, RN, BSN
From the notes of:John Nation, RN, MSNCharlene Morris, RN, MSNKelle Howard, MSN. RN, CNE
Cirrhosis Facts:Progressive, leads to liver failureInsidious, prolonged course9th leading cause of death in U.S.Twice as common in menHighest incidence between ages 40 and 60.
What is Cirrhosis?Extensive destruction of liver cellsCells attempt to regenerateRegenerative process is disorganizedFunctional liver tissue is destroyed and
scarring of liver occursOvergrowth of fibrous connective
tissue, distorting liver structure; obstructing blood flow
Four Types of Cirrhosis:
Alcoholic formerly called ________
Post-necrotic Biliary/obstructive Cardiac
Alcoholic cirrhosis:Usually associated with alcohol abuseMost common cause of cirrhosisCauses metabolic changes in liver
fat accumulates in liver (fatty liver)Fatty liver potentially reversibleIf alcohol abuse continues, widespread
liver scar formation occurs
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
Biliary cirrhosis:
Associated with chronic biliary obstruction and/or
infectionPrimary sclerosing cholangitis?
Diffuse fibrosis of liver
Jaundice is main feature
www.humanillnesses.com
Cardiac cirrhosis:
Develops from long-standing right sided heart failure
Results in patients with cor-pulmonale, constrictive pericarditis, and tricuspid insufficiency
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
Early Signs of cirrhosis: Nausea and vomiting Anorexia Diarrhea or constipation Pain Fever Weight loss
Later Manifestations:
JaundiceSkin Lesions/Spider angiomasPalmer erythemaThrombocytopenia, Leukopenia, Anemia Coagulation disordersEndocrine disturbancePeripheral neuropathy & peripheral edema
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)
Skin Lesions
• WHY?
• Dilated blood vessels (spider angiomas)
• Palmar erythema
Hematologic Problems Thrombocytopenia Leukopenia Anemia Vitamin K deficiency
www.elements4health.com
Endocrine Problems: Inactivation of adrenocortical
hormones Men Women Hyperaldosteronism
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
Esophageal & Gastric Varices
Peripheral Edema & Ascites
Hepatic Encephalopathy
Complications:Portal Hypertension
• Compression and destruction of portal & hepatic veins
• Increased venous pressure in portal circulation
• Characterized by:• Collateral circulation develops
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!!
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?
Sengstaken-Blakemore Tube
Three Lumens:Esophageal balloon
inflationGastric balloon
inflationGastric aspiration
Acute BleedSupportive 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!!
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
TIPS Transjugular intrahepatic
portosystemic shunt
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
Increased capillary
permeability
Increased Na+
&H2O retention
Portal Hypertension
HypoproteinemiaFour Factors Lead to Ascites
www.patient.co.uk
Nursing Management of ASCITES:
Assess for respiratory distress Fowler’s position helps ease
work of breathingDaily weightsMeasure abdominal girthAccurate I&O
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
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
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 manifestationshttp://chemistry.about.com
Where does ammonia come from?
A by-product of protein metabolismProtein and amino acids are broken
down by bacteria in GI tract, producing ammonia.
Liver converts this to urea which is eliminated in the urine
Hepatic Encephalopathy Stages0-1st
InsomniaPersonality
changesDisturbances of
awarenessForgetfulness,
irritability, & confusion
Trouble writing
http://lukeromyn.com/blog
Hepatic Encephalopathy Stages
2nd & 3rdLethargy, drowsinessInappropriate speech
Slurred speechDisorientationAsterixis
flapping tremorsHiccupsHyperactive reflexesViolent behavior Slow, deep respirationsFetor hepaticus
musty sweet smell to breath
Hepatic Encephalopathy Stages
4th + Babinski
Possible seizures
Swelling of brain tissue
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)
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
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
Overall Goals: Relief of discomfort Minimal to no complications
(ascites, varices, hepatic encephalopathy)
Return to normal as possible lifestyle
http://www.fontana.org/index
Liver Dialysis
Bridge to transplantDialyze 6 hours at a time
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.
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
http://www.murketing.com/journal