Transcript Cirrhosis ppt - print and bring to class

Cirrhosis
Ashley Valentino
Fall 2013
From the notes of:
John Nation, RN, MSN
Charlene Morris, RN, MSN
Austin Community College
Cirrhosis Facts:
 Progressive, leads to liver failure
 Insidious, prolonged course
 What does this mean?
 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
» Causes what?
• 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 Laennec’s
• 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
– How?
• If alcohol abuse continues, widespread liver scar
formation occurs
 What actually causes it?
Post Necrotic cirrhosis:
• Complication of:
– viral infections
– Toxicity
• Which medications?
– autoimmune hepatitis
• 20% of of patient’s with chronic hepatitis C will
develop cirrhosis
• Broad bands of scar tissue form within the liver
• Hep C + ___________= inc. the rate of cirrhosis?
Biliary cirrhosis:
 Associated with chronic biliary obstruction and/or
infection
Primary sclerosing cholangitis?
What is this?
 Diffuse fibrosis of liver
 Jaundice is main feature
 What actually causes it?
www.humanillnesses.com
Cardiac cirrhosis:
• Develops from long-standing right sided heart failure
• Results in patients with cor-pulmonale, constrictive
• pericarditis, and tricuspid insufficiency
What actually causes it?
How do you treat this type?
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 – why?
Early Signs of cirrhosis:
 Nausea and vomiting
 Anorexia
 Diarrhea or constipation
 Pain

Where? Why?
 Fever
 Weight loss
•
•
WHY?
How do you know when cirrhosis begins?
Later Manifestations:
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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
aka:___________
• WHY?
• Dilated blood vessels (spider angiomas)
• Palmar erythema
•
What is this?
Hematologic Problems
 Thrombocytopenia

Why?
 Leukopenia

Why?
 Anemia

Why? What are some s/s to teach?
 Vitamin K deficiency

Why is this significant?
www.elements4health.com
Endocrine Problems:
 Inactivation of adrenocortical hormones

Which ones?
 Men


What s/s will you see?
Related to what?
 Women


What s/s will you see?
Related to what?
 Hyperaldosteronism

Causes what?
Peripheral Neuropathy
&
Peripheral Edema
 Neuropathies- from what?
• Results in mixed nervous symptoms
• Sensory symptoms are most common
 Edema
•
Caused by what?
Complications:
 Portal Hypertension
 Esophageal & Gastric Varices
 Peripheral Edema & Ascites
 Hepatic Encephalopathy
Complications:
Portal Hypertension
• Compression and destruction of portal &
hepatic veins
•
How much blood carried by portal vein? To where?
• Increased venous pressure in portal circulation
• Characterized by:
•
What?
• Collateral circulation develops
•
Why?
•
o
Resulting in:
•
Varices?
•
Caput Medusae?
What is the most serious complication of portal hypertension?
Ascites & Caput medusae
Complications:
Esophageal & Gastric Varices:
o Esophageal:
•
•
complex of twisting veins at lower end of esophagus
enlarged & swollen
o Gastric:
•
•
upper portion of stomach
may occur alone or in combination with esophageal
o Tolerate high pressure poorly, bleeding easily
with distention
o Rupture in response to irritation- factors?
o
What will we teach?
o Most life threatening complication!!
Treatment for Varices:
o Stop bleeding, manage airway, prevent aspiration of blood!!
•
How will you prevent aspiration?
o Drug Therapy:
•
Propranolol, Sandostatin, Vasopressin, NTG
•
How do these work?
o Band ligation of varices
o Endoscopic sclerotherapy
•
Thromboses and obliterates distended veins
o Balloon tamponade-mechanical compresson of varices
•
Sengstaken-Blakesmore
o Avoid:
•
alcohol & irritating foods
•
What common drugs should be avoided?
Band Ligation
Sclerotherapy:
• A sclerosant solution
(ethanolamine oleate or
sodium tetradecyl
sulphate) is injected into
the bleeding varix or the
overlying submucosa
• Complications can
include fever, dysphagia
and chest pain,
ulceration, stricture, and
(rarely) perforation.
SengstakenBlakesmore
Sengstaken-Blakemore Tube
Three Lumens:
• Esophageal balloon
inflation
• Gastric balloon inflation
• Gastric aspiration
• What are some interventions
related to this tube?
Acute Bleed
Supportive Measures:
o
o
o
o
FFP, PRBC’s, Vitamin K – why?
Antibiotics
Protonix, Zantac – why?
Propanolol
•
How does it work?
o Prevent factors that may increase intra-abdominal
pressure!!
•
Like what? What are some interventions?
o 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
• WHY?
TIPS:
Transjugular intrahepatic
portosystemic shunt
Complications:
Ascites & Peripheral Edema
o Results from impaired liver synthesis of
albumin = hypoalbuminemia
o Occurs as ankle and presacral edema
o Ascites:
•
•
accumulation of serous fluid in periotoneal or
abdominal cavity
Spontaneous bacterial peritonitis (SBP)
o Hyperaldosteronism
•
Results in what?
Four Factors Lead to Ascites
Hypoproteinemia
Increased Na+
&
Increased
capillary
permeability
H2O retention
Portal Hypertension
Accumulation of high protein fluid in the abdomen
Nursing Management of
ASCITES:
o Assess for respiratory distress
• Fowler’s position helps ease work
of breathing
o Daily weights
o Measure abdominal girth
o Accurate I&O
Medical Management of Ascites:
o Na+ and Fluid restriction
•
How much?
o Albumin
•
Why?
o Diuretic therapy:
•
Aldactone, HCTZ, Lasix
•
•
What is the difference between these?
Which do you think would most appropriate?
o Paracentesis
•
•
needle puncture of abdominal cavity to remove ascitic
fluid- temporary
have patient void before procedure
o What may be given IV prior to procedure?
o Nursing care post procedure?
Management of Ascites:
o Peritoneovenous Shunt
•
•
•
•
surgical procedure
provides continuous reinfusion of ascitic fluid
into venous system
Not 1st line in therapy due to high # of
complications – such as?
Does not improve survival rates
Hepatic Encephalopathy:
o Terminal complication of liver disease
o Disorder of protein metabolism and excretion
o Ammonia
•
•
enters the systemic circulation without liver
detoxification
crosses blood-brain barrier, causing neurologic
toxic manifestations
o Four stages of manifestations
• Review Table 44-12 (page 1077)
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
Early Stages
0-1
•
•
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•
•
•
•
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Insomnia
Sleep disturbances
Short attention span
Tremors, incoordination
Personality changes
Depression
Disturbances of awareness
Forgetfulness, irritability, &
confusion
• Trouble writing
• Asterixis
Hepatic Encephalopathy
Stages
2nd & 3rd
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Lethargy, drowsiness
Slow and slurred speech
Disorientation
Asterixis
Impaired judgement
Hyperactive reflexes
Violent behavior
Slow, deep respirations
+ Babinski reflex
Fetor hepaticus – what is this?
Hepatic Encephalopathy
Stage 4
Impending Coma
• + Babinski
• Not rousable
• May be responsive to
painful stimuli
• Decerebrate
• Possible seizures
Treatment:
Hepatic Encephalopathy
o Reduce ammonia formation
•
Lactulose
•
•
How does this work?
How is it given?
o Control GI bleeding – why?
o Decreasing protein in intestine
o Neomycin
•
What is this? How does it work?
o Electrolyte replacement
•
Which ones?
o Possible liver transplant
•
depends on a number of factors
Hepatorenal Syndrome:
o Serious complication
o Functional renal failure with advancing
azotemia, oliguria, and ascites
•
what will we see in regards to labs?
o Portal hypertension + liver decompensation
= decreased arterial blood volume & renal
vasoconstriction
o May be reversed by liver transplantation
Nutritional Therapy:
 High calorie/High Carb diet
 Low protein diet – when?
 Parenteral nutrition of tube feedings
may be required
 Low-sodium diet – when?
 Dietary education on reading labels at
home
Overall Goals:
 Relief of discomfort
 Minimal to no complications
• ascites, varices, hepatic encephalopathy
 Return to normal as possible lifestyle
Liver Dialysis
o Bridge to transplant (introduced in 1999)
• Utilizes charcoal as detoxifying agent
o Dialyze 2-5 days in a row
o Dialyze 4- 6 hours at a time
Liver Transplantation
o Blood type and body size are critical factors in determining
who is an appropriate donor.
o 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.
o Cadaver vs. live donor livers
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 Transplant
complications
o Rejection. About 70% of all liver-transplant patients have some
degree of organ rejection prior to discharge
• Anti-rejection medications are given to ward off the immune attack
o Infection
• Most infections can be treated successfully as they occur
o Cancer
http://www.google.com/imgres?imgurl=http://1.bp.blogspot.com/_huyc4ygeN9o/SERUOrRU07I/AAAA
AAAAAcI/zwWQfN0Q9jM/s320/x_scar.gif&imgrefurl=http://mrcppreview.blogspot.com/2008/06/scarag
ain.html&h=221&w=320&sz=39&tbnid=GpI65e7ofQWymM:&tbnh=90&tbnw=130&zoom=1&usg=__nk4
4z547W0qi8k6hFUZkjF291QI=&docid=5Vu2gOCl3TOdM&hl=en&sa=X&ei=CiIQUdr3O6PE2gXxnoCQDw&ved=0CDUQ9QEwAQ&dur=44
http://www.organdonor.gov/about/transplantationprocess.html
Organ
Hearts
Lungs
Livers
Kidneys
Pancreata
Intestine
Median national
waiting time
113 days
141 days
361 days
1,219 days
260 days
159 days
Review Questions:
1. A priority of care for a client having a
paracentesis is to?
A. Force fluids, instruct patient to keep
bladder full prior to procedure
B. Instruct patient on how to cough
during procedure
C. Assist patient into supine position with
feet elevated
D. Monitor patient’s BP during and after
procedure
2. After receiving shift report, which of
the following patients would you see
first?
A. 56 year old with Hepatitis B and D
B. 58 year old male, recently diagnosed
with hepatic cancer
C. Patient with esophageal varices
treated with sclerotherapy this AM.
D. Patient with splenomegaly, anemia,
and PLT count of 60,000
3. A client with cirrhosis is receiving
lactulose (Cephulac). During the
assessment, the nurse notes increased
confusion and asterixis. The nurse should:
A. Assess for GI bleeding
B. Hold the lactulose (Cephulac)
C. Increase protein in the diet
D. Monitor serum billirubin levels
http://www.murketing.com/journal