Cirrhosis by

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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
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.
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
Four Types of Cirrhosis:
 Alcoholic
 formerly called ________
 Post-necrotic
 Biliary/obstructive
 Cardiac
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
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
infection
Primary 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:
 Jaundice
 Skin Lesions/Spider angiomas
 Palmer erythema
 Thrombocytopenia, Leukopenia, Anemia
 Coagulation disorders
 Endocrine disturbance
 Peripheral 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-Blakesmore
www. medical-dictionary.com
Sengstaken-Blakemore Tube
Three Lumens:
 Esophageal balloon
inflation
 Gastric balloon
inflation
 Gastric aspiration
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!!
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
Four Factors Lead to Ascites
Hypoproteinemia
Increased Na+
&
Increased
capillary
permeability
H2O retention
Portal Hypertension
www.patient.co.uk
Nursing Management of ASCITES:
 Assess for respiratory
distress

Fowler’s position helps ease
work of breathing
 Daily weights
 Measure abdominal girth
 Accurate 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 manifestations
http://chemistry.about.com
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
Hepatic Encephalopathy
Stages
0-1st
 Insomnia
 Personality changes
 Disturbances of
awareness
 Forgetfulness,
irritability, &
confusion
 Trouble writing
http://lukeromyn.com/blog
Hepatic Encephalopathy
Stages
2nd & 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
Hepatic Encephalopathy
Stages
th
4
 + 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 transplant
 Dialyze 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
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