Transcript Hepatitis B - Austin Community College

Liver Disorders
Part 1
Charlene Morris, RN, MSN
Austin Community College
Addenda Spring 2010 John Nation RN, MSN
Have you finished reading
the Lewis text?
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Overview of Today’s Lecture
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A & P Review
Hepatitis A
Hepatitis B
Hepatitis C
Cirrhosis
Portal Hypertension
Esophageal Varices
Hepatic Encephalopathy
Hepatorenal Syndrome
Liver Transplant
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Which letter points to the
liver?
A and P Review
A and P Review
Largest internal organweighs around 3 lbs!
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A
B
C
D
E
Liver
Hepatic vein
Hepatic artery
Portal vein
Common bile
duct
F Stomach
G Cystic duct
H Gallbladder
Blood Supply – 2 sources
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Hepatic artery – 500cc/min oxygenated
blood.
– 30% of Cardiac output goes to the liver
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Portal vein – 1000cc/min partly oxygenated
blood supplies 50 - 60% O2 plus rich supply of
nutrients, toxins, drugs
stomach, small and large intestines, pancreas and
spleen
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Both empty into capillaries/sinusoids
Liver filters the blood
Hepatic vein to inferior vena cava
Hepatic Circulation Video
Lobule –
Functional unit of the liver
Capillaries
Metabolic Functions of
the liver
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“Body’s Refinery” Over 400 functions
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Primary role in anabolism and catabolism
Metabolic Functions of the Liver
1. Metabolism of Glucose - glucose buffer
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When glucose levels rise
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liver stores it as glycogen
When glucose levels low
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Liver breaks glycogen to usable glucose
Amino acids to glucose
Fatty acids/triglycerides into glucose
2. Protein – major storage center for protein
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When protein storage at full capacity, liver breaks it into
glucose then forms glycogen and fatty acids for storage
Breakdown of amino acids releases ammonia
Liver converts ammonia to urea and excreted by the kidneys
Metabolic Functions of the liver cont.
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Fatty acids – Conversion of triglycerides into fatty acids &
glycerol by enzymes in capillary walls of liver and adipose tissue
- Digestion & Storage of fats
- Energy
Glycerol and fatty acids can enter the Kreb’s cycle.
Some triglycerides break down/are converted to new glucose
releasing ketones
Released Ketones can fuel heart & skeletal muscles/ lower pH
4. Cholesterol
– produced by the liver & used for fat digestion
- processed into lipoproteins
LDL metabolized – releases oxygen free
radicals/electrons – vessel & cell damage
HDL carries cholesterol from cells back to the liver
Other functions
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Immunologic – phagocytic Kupffer’s cells in liver remove
bacteria, dead cells and other foreign substances from blood
Blood storage
– Emergency reserve
– may be up to 400-500cc with Rt. Heart failure
Plasma protein synthesis
- including albumin for maintaining plasma osmotic
pressure
Clotting
– factor synthesis fibrinogen, prothrombin and
factor VII
- absorption of vitamin K
Storage of vitamins and minerals
– B12, D, and A
– Iron as ferritin
Other transformation processes
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Waste products of hemoglobin - transformed
to a water-soluble form of Bilirubin that can be
excreted
Indirect/unconjugated bilirubin is attached to albumin, goes to the
liver to be changed to direct/conjugated water soluble form.
Conjugated bilirubin is soluble and excreted in bile. A small amount is
reabsorbed by the blood.
Formation and secretion of bile
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Contains cholesterol and bile salts for digestion of fats.
Used in fat soluble vitamin absorption
Bile transports bilirubin to the intestines to be excreted
In the intestines, bacteria convert conjugated bilirubin to
stercobilinogen and urobilinogen
Stercobilinogen causes brown color of stool
Some urobilinogen is reabsorbed into blood, returned to liver, and
excreted as bile.
Other transformation
processes
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Steroids and hormones - acts on
these to make them water soluble for
excretion – otherwise would
concentrate in body tissues
Ammonia – neurotoxic byproduct of
protein breakdown transformed into
urea for excretion in urine
Drugs, alcohol and toxins
metabolism– transforms to water
soluble for excretion
To Summarize….
The liver:
– changes food into energy
– removes alcohol and poisons from the
blood
– makes bile, a yellowish-green liquid that
helps with digestion
Hepatitis
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Simply means inflammation of the liver
– “itis” means inflammation, “hepa” means
liver.
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Viral hepatitis
– Most common cause
– Viral types include A, B, C, D, E, and G
Hepatitis
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Other possible causes
– Drugs (alcohol)
– Chemicals
– Autoimmune liver disease
– Bacteria (rarely)
Hepatitis
Etiology
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Causes
– A, B, C, D, E, and G virus
– Cytomegalovirus
– Epstein-Barr virus
– Herpes virus
– Coxsackievirus
– Rubella virus
Hepatitis A
Etiology
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Hepatitis A virus (HAV)
– RNA virus
– Transmitted fecal–oral route, parenteral
(rarely)
– Frequently occurs in small outbreaks
Hepatitis A
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61,000 cases of hepatitis A occur
annually in the United States
10 million cases of hepatitis A occur
worldwide
– Nearly universal during childhood in
developing countries
Hepatitis Statistics- CDC
Hepatitis A
Etiology
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Hepatitis A virus (HAV)
– Found in feces 2 or more weeks before
the onset of symptoms and up to 1 week
after the onset of jaundice
– Present in blood briefly
– No chronic carrier state
Incubation Period
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2-6 weeks
Acute onset
Mild flu-like manifestations
Symptoms last up to 2 months
Liver usually repairs itself, so no
permanent effects
Hepatitis A
Etiology
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Hepatitis A virus (HAV)
– Anti-HAV immunoglobulin M (IgM)
Appears in the serum as the stool becomes
negative for the virus
 Detection of IgM anti-HAV indicates acute
hepatitis
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Hepatitis A
Etiology
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Hepatitis A virus (HAV)
– Anti-HAV immunoglobulin G (IgG)
IgG anti-HAV: Indicator of past infection
 Presence of IgG antibody provides lifelong
immunity
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Mode of Transmission
HAV
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Mainly by ingestion of food or
liquid infected with the virus
–Poor hygiene, improper handling
of food, crowding housing, poor
sanitation conditions are all
factors related to Hepatitis A
Mode of Transmission
HAV
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Occurs more frequently in
underdeveloped countries
Contaminated waters
–Drinking water, contaminated
seafood
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Food-borne Hepatitis A outbreaks
usually due to infected food handler
–Contamination of food during
preparation
Hepatitis A Vaccine
2
doses IM
–Initial dose
–Booster in 6 to 12
months
Post-exposure
Prophylaxis
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Standard IG-immune globulin
– Given IM within 2 weeks of exposure
Hepatitis A Vaccine
IG is recommended for persons who do not have
anti-HAV antibodies and have had food borne
exposure or close contact with HAV-infected person
Remember 2/2/2/2 Rule
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2 doses IM to prevent
Signs & symptoms last 2 months
Contagious 2 weeks before signs &
symptoms
Post-exposure dose given IM within 2 weeks
of exposure
Must report within one day
Hepatitis B
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Nearly 400 million people infected with
Hepatitis B
– 50% to 75% active viral replication
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73,000 new cases of Hepatitis B
annually in United States
– Incidence decreased due to HBV vaccine
Hepatitis B
Etiology

Hepatitis B virus (HBV)
– DNA virus
– Transmission of HBV
Perinatally by mothers infected
 Percutaneously (IV drug use)
 Horizontally by mucosal exposure to infectious
blood, blood products, or other body fluids
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Hepatitis B
Etiology
 Hepatitis
B virus (HBV)
–Transmission occurs when
infected blood or other body
fluids enter the body of a
person who is not immune to
the virus
Hepatitis B
Etiology
 Hepatitis
B virus (HBV)
– Sexually transmitted disease
– Can live on a dry surface for 7 days
– More infectious than HIV
Hepatitis B- Precautions
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PREVENT INFECTION OF FAMILY — Acute and chronic hepatitis B are
contagious. Thus, people with hepatitis B should discuss measures to reduce
the risk of infecting close contacts. This includes the following:
Discuss the infection with any sexual partners and use a latex condom with
every sexual encounter.
Do not share razors, toothbrushes, or anything that has blood on it.
Cover open sores and cuts with a bandage.
Do not donate blood, body organs, other tissues, or sperm.
Immediate family and household members should have testing for hepatitis B.
Anyone who is at risk of hepatitis B infection should be vaccinated, if not
done previously. (See "Patient information: Adult immunizations".)
Do not share any injection drug equipment (needles, syringes).
Clean blood spills with a mixture of 1 part household bleach to 9 parts water.
Source: UptoDate
Hepatitis B- Prevention
Hepatitis B cannot be spread by:
 Hugging or kissing* (some disagreement)
 Sharing eating utensils or cups
 Sneezing or coughing
 Breastfeeding
Source: Uptodate
Hep B Incubation Period
 6-24
weeks
 Prevention
–Vaccine-3 doses
Initial
dose
Dose at 4 weeks
Dose 5 months later
Post-exposure Hep B
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Hepatitis B Immune globulin
IM in 2 doses
– First dose within 24 hours to 7 days of
exposure
– Second dose 20 to 30 days post-exposure
Provides short-term immunity
Give HBV vaccine concurrently- vaccine can
be beneficial post- exposure
Hepatitis B
Etiology
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Hepatitis B virus (HBV)
– Complex structure with three antigens
 Surface antigen (HBsAg)
 Core antigen (HBcAg)
 E antigen (HBeAg)
– Each antigen—a corresponding antibody
may develop in response to acute viral
Hepatitis B
Hepatitis B Virus
Etiology
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Presence of Hepatitis B Surface
Antibodies
– Indicates immunity from HBV vaccine
– Past HBV infection
– With chronic infection, liver enzyme
values may be normal or ↑
– 15% to 25% of chronically infected
persons die from chronic liver disease
Hepatitis C
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Approximately 170 million people are
infected with the hepatitis C virus
(HCV)
Estimated 30,000 new cases
diagnosed annually
Hepatitis C
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8000 to 10,000 people in the
United States die each year from
complications of end-stage liver
disease secondary to HCV
Approximately 30% to 40% of
HIV-infected patients also have
HCV
Hepatitis C
Etiology
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Hepatitis C virus (HCV)
– Transmitted percutaneously
– Risk factors
 IV drug use
–Most common mode of
transmission in United States
and Canada
 Blood transfusions
Hepatitis C
Etiology
 Hepatitis
C virus (HCV)
–Risk factors (cont’d)
– High-risk sexual behavior
 Hemodialysis
 Occupational
exposure
 Perinatal transmission
Hepatitis C
MOT
 Hepatitis
C virus (HCV)
– Up to 10% of patients with HCV cannot
identify a source
– Risk of body piercings, tattooing, and
intranasal drug use in transmission of
HCV
Hepatitis C
Diagnostic Studies
Anti-HCV
HCV
RNA
antibody
You Tube Hepatitis C
Hepatitis C Interventions
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Needle Exchange
Harm Reduction - Austin Harm
Reduction Coalition
Hepatitis D
Etiology
 Hepatitis
D virus (HDV)
– Also called delta virus
– Defective single-stranded RNA virus
– Cannot survive on its own
– Requires the helper function of HBV
to replicate
Hepatitis D
Etiology
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Hepatitis D virus (HDV) (cont’d)
–HBV-HDV co-infection
 ↑ Risk of fulminant hepatitis
More severe acute disease
Hepatitis E
Etiology
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Hepatitis E virus (HEV)
– RNA virus
– Transmitted fecal–oral route
– Most common mode of transmission
is drinking contaminated water
– Occurs primarily in developing
countries
Hepatitis G
Etiology
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Hepatitis G virus (HGV)
–RNA virus
–Poorly characterized parenterally
and sexually transmitted virus
–Found in some blood donors
–Can be transmitted by blood
transfusion
Hepatitis G
Etiology
 Hepatitis
(cont’d)
G virus (HGV)
–Coexists with other hepatitis
viruses and HIV
–Does not appear to cause liver
damage
Pathophysiology of
Hepatitis
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Acute infection- widespread
inflammation of liver tissue
– Liver damage mediated by
 Cytotoxic cytokines
 Natural killer cells
– Liver cell damage results in hepatic
cell necrosis
Common Manifestations
of Acute Hepatitis
 Predictable
course among all
the viruses
 Incubation Phase: after
exposure to virus, no
symptoms
Preicteric Phase of
Hepatitis
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Flu-like symptoms
–General malaise
–Fatigue
–Body aches, headache
–GI symptoms- nausea/vomiting,
diarrhea, abdominal discomfort
–Chills, low grade fever
Icteric or Jaundice Phase
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Usually 5-10 days after pre-icteric symptoms
Jaundice results when bilirubin diffuses into
tissues
Sclera jaundiced
Urine darkens due to excess bilirubin being
excreted
If bilirubin cannot flow out of liver, stool will
be light or clay-colored
Severe Jaundice
Hepatitis
Clinical Manifestations
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Pruritus can accompany jaundice
– Accumulation of bile salts beneath the
skin
When jaundice occurs, fever subsides
Liver usually enlarged and tender
Convalescent Phase
Healing generally within 3-16
weeks
 Begins as jaundice is disappearing
 GI symptoms minimal
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Hepatitis
 Liver
cells can regenerate with
time and if no complications
occur, resume their normal
appearance and function
Hepatitis
Complications
 Fulminant
Hepatic Failure
 Chronic Hepatitis
 Cirrhosis
 Hepatocellular Carcinoma
Fulminant Hepatitis
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Results in severe impairment or necrosis of
liver cells and potential liver failure
Develops in small percentage of patients
Occurs because of
 Complications of Hepatitis B
 Toxic reactions to drugs and congenital
metabolic disorders
Diagnostic tests
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Liver function studies
– ALT (Alanine aminotransferase) – elevates: enzyme
in liver cells released into bloodstream with injury or
disease (0 – 50) normal
– AST (Aspartate aminotransferase) – elevates: enzyme
in liver & heart cells released into bloodstream (0 -41)
– GGT – gamma glutamyltransferase: present in all cell
membranes, inj or disease = elevates in cell lysis, (8
– 55). increases when bile ducts are blocked &
hepatitis. Elevated until function returns.
Diagnostic tests
– Alkaline phosphatase – present in liver & bone
cells. Elevated in hepatitis.(44-147 IU/L)
– CBC – low RBC, Hct, Hgb related to anemia, RBC
destruction, bleeding, folic acid and vitamin
deficiencies.
– Low WBC and Platelets
 Increased blood flow to spleen – cells destroyed
faster than needed
– AFP- alpha fetoprotein– liver cancer marker
– Lactic dehydrogenase LDH5 specific for liver damage
Diagnostic tests
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Coagulation – prolonged prothrombin
time due to poor production of
prothombin by liver and decreased
Vitamin K absorption (Normal PT 12-15
seconds, INR 0.8 to 1.2)
Hyponatremia –hemodilution
Hypokalemia, hypophosphatemia,
hypomagnesemia –malnutrition & renal
loss
Bilirubin – Total (2-14 umol/L)
Bilurubin – direct/conjugated (0-4 umol/L)
Diagnostic tests
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Serum albumin – low due to impaired
liver production (3.3 – 5)
Serum ammonia – high (0 – 150)(10 to
80 ug/l)
Glucose and cholesterol –abnormal due
to impaired liver function
Abd. Ultrasound – liver size, ascites, or
nodules
Esophagascopy – look for varices
Liver biopsy
CT, MRI
Rx impacting liver
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A host of medications can cause abnormal liver enzymes levels.
Examples include:
Pain relief medications such as aspirin, acetaminophen (Tylenol),
ibuprofen (Advil, Motrin), neproxen (Narosyn), diclofenac (Voltaren),
and phenylbutazone (Butazolidine)
Anti-seizure medications such as phenytoin (Dilantin), valproic acid,
carbamazepine (Tegretol), and phenobarbital
Antibiotics such as the tetracyclines, sulfonamides, isoniazid (INH),
sulfamethoxazole, trimethoprim, nitrofurantoin, etc.
Cholesterol lowering drugs such as the "statins" (Mevacor, Pravachol,
Lipitor, etc.) and niacin
Cardiovascular drugs such as amiodarone (Cordarone), hydralazine,
quinidine, etc.
Anti-depressant drugs of the tricyclic type (ie elavil)
With drug-induced liver enzyme abnormalities, the enzymes usually
normalize weeks to months after stopping the medications.
3 Types of Liver Biopsy
Needle biopsy
Most common in past
Laparoscopic biopsy:
Used to remove tissue from specific parts of the liver.
Transvenous biopsy
•Catheter into a vein in the neck and guiding it to the liver.
•A biopsy needle is placed into the catheter and advanced
into the liver.
•Used for patients with blood-clotting problems or excess
fluid
Liver Biopsy
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Adequacy of clotting- PT/ INR, Platelets (Vit. K?)
Type and cross match for blood
Usually hold aspirin, ibuprofen, and
anticoagulants
Chest x-ray
Consent form & NPO 4 to 8 hr.
Vital signs & Empty bladder
Supine position, R arm above head
Hold breath after expiration when needle
inserted
Be very still during procedure – 20 minutes
Liver Biopsy Video
Complications are:
Puncture of lung or gallbladder, infection, bleeding, and pain.
After Needle Liver Biopsy
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Pressure to site, place pt on Rt side to maintain site
pressure minimum of 2 hrs. & flat 12-14 hrs.
Vital signs & check for bleeding
NPO X 2H after
Assess for peritonitis, shock, & pneumothorax
Rt. shoulder pain common
– caused by irritation of the diaphragm muscle
– usually radiates to the shoulder a few hours or days.
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Soreness at the incision site
Avoid aspirin or ibuprofen for pain control for the first
week because they decrease blood clotting, which is
crucial for healing. CONSULT HEALTHCARE PROVIDER!
Avoid coughing, straining, lifting x 1-2 weeks
Hepatitis Care
 Rest
is a priority!
 Diet –High calorie & protein, Low
fat
–Vitamin supplement – B
complex & K
–Avoid alcohol & drugs detoxed
in liver
 Life style changes
Meds for Chronic
Hepatitis
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Chronic HBV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Lamivudine (Epivir)
 Adefovir (Hepsera)
 Entecavir (Baraclude)
 Telbivudine (Tyzeka)
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Chronic HCV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Ribavirin (Rebetol, Copegus)
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Hepatitis
Nursing Management
Nursing assessment
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Past health history
– Hemophilia
– Exposure to infected persons
– Ingestion of contaminated food or water
– Past blood transfusion (before 1992)
Hepatitis
Nursing Management
Nursing assessment
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Medications (use and misuse)
– Acetaminophen
– Phenytoin
– Halothane
– Methyldopa
Hepatitis
Nursing Management
Nursing assessment
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IV drug and alcohol abuse
Weight loss
Dark urine
Fatigue
Right upper quadrant pain
Pruritus
Hepatitis
Nursing Management
Nursing assessment
 Low-grade
fever
 Jaundice
 Abnormal
laboratory values
Hepatitis
Nursing Management
Nursing diagnoses
Imbalanced nutrition: Less than
body requirements
 Activity intolerance
 Ineffective therapeutic regimen
management
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Hepatitis
Nursing Management
 Overall
goals: Planning
–Relief of discomfort
–Resumption of normal activities
–Return to normal liver function
without complications
Hepatitis
Nursing Management
Nursing implementation
 Health
promotion
–Hepatitis A
Education
Vaccination
Good hygiene practices
Hepatitis
Nursing Management
Nursing implementation
Health Promotion
–Hepatitis B
Vaccination
 Education
 Workplace safety

Hepatitis
Nursing Management
Nursing implementation
 Health
promotion
–Hepatitis C
Education
 Infection control precautions
 Modification of high-risk behavior
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Hepatitis
Nursing Management
Nursing implementation
 Acute
intervention
–Rest
–Jaundice
Assess degree of jaundice
Small, frequent meals
Hepatitis
Nursing Management
Nursing implementation
 Ambulatory
and home care
–Dietary teaching
–Assessment for complications
–Regular follow-up for at least
1 year after diagnosis
Hepatitis
Nursing Management
Nursing implementation
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Ambulatory and home care
–Avoid alcohol
Hepatitis
Nursing Management
Evaluation
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Expected outcomes
–Adequate nutritional intake
–Increased tolerance for activity
–Verbalization of understanding
of
follow-up care
Hepatitis
Nursing Management
Evaluation
 Expected
outcomes
–Able to explain methods of
transmission and methods of
preventing transmission to
others
Hepatitis Reporting
Which type of hepatitis has
few long term consequences?
25% 25% 25% 25%
D
H
ep
at
iti
s
C
H
ep
at
iti
s
B
H
ep
at
iti
s
A
4.
at
iti
s
3.
A
B
C
D
ep
2.
Hepatitis
Hepatitis
Hepatitis
Hepatitis
H
1.
Which statement about
hepatitis is true?
at
iti
s
ep
H
be
a
is
D
C
at
iti
s
ep
H
ni
g.
..
ns
m
...
is
tr
a
is
B
at
iti
s
ep
H
tr
a
ns
m
i..
.
d.
..
le
a
n
of
te
A
4.
at
iti
s
3.
ep
2.
Hepatitis A often leads
to fulminant hepatitis
Hepatitis B is
transmitted via blood
and other body fluids
Hepatitis C is
transmitted via fecaloral route
Hepatitis D is a benign
infection
H
1.
25% 25% 25% 25%
Which types of hepatitis
have vaccines?
25% 25% 25% 25%
E
,C
,&
B
at
iti
s
H
ep
ep
H
ep
H
at
iti
s
at
iti
s
B
A
&
&
C
B
C
,B
,&
A
4.
at
iti
s
3.
A, B, & C
A&B
B&C
B, C, & E
ep
2.
Hepatitis
Hepatitis
Hepatitis
Hepatitis
H
1.
Juandice occurs during
which stage of hepatitis?
1.
2.
3.
4.
Incubation
Pre-icteric
Icteric
Post-icteric
Break!!
Cirrhosis Video Clip
Cirrhosis
Cirrhosis Pathophysiology
Cirrhosis is the end stage of
chronic liver disease
 Progressive, leads to liver failure
 Insidious, prolonged course
 Ninth leading cause of death in
United States
 Twice as common in men
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Cirrhosis Pathophysiology
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Hepatocytes are destroyed and portal
hypertension develops
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Liver cells attempt to regenerate
Regenerative process is disorganized
Functional liver tissue is destroyed and
scarring of liver occurs
New fibrous connective tissue distorts
liver’s normal structure, with impeded
blood flow
Four Types of Cirrhosis
 Alcoholic
Cirrhosis – formerly
called Laennec’s
 Post necrotic Cirrhosis
 Biliary/obstructive - bile flow
obstructed causing damage to
liver
 Cardiac- from right side heart
failure
Alcoholic or Nutritional Cirrhosis
(formerly called Laennec’s)
 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 consumption ceases
Post Necrotic Cirrhosis
Results from complication of viral
infections, Hepatitis, or exposure to
toxins
Liver shrinks because lobules destroyed,
broad bands of scar tissue form within
the liver
Biliary Cirrhosis
 Associated
with chronic biliary
obstruction and infection
 Retained bile damages and destroys
liver cells, causing fibrosis of liver
Cardiac Cirrhosis
Results from long-standing severe right
sided heart failure
Elevated central venous pressures cause
stasis of blood in veins of liver, which
leads to fibrosis
Early Signs of Cirrhosis
Complications
and Common Manifestations
1. Hepatomegaly and RUQ pain
2. Weight loss
3. Weakness
4. Anorexia
5. Diarrhea and constipation
Cirrhosis Interventions-
Drugs





Diuretics– Aldactone (spironolactone): decreases aldosterone
levels, K+ sparing
– Lasix (furosemide)
Salt-poor albumin
Neomycin – decrease ammonia forming organisms.
Only recommended when unable to tolerate lactulose
Lactulose – decreases ammonia forming organisms
and inc. acidity of bowel. Goal is 2-3 loose stools per
day.
Ferrous sulfate and folic acid – to treat anemia/
vitamin deficiency



Beta blocker: propranolol (Inderal),
nadolol- to prevent bleeding of E varices
in conjunction with isosorbide
mononitrate (Imdur) lowers hepatic
venous pressure
Proton Pump Inhibitors, H2 Receptor
Blockers– decrease irritation of varices
Serax (oxazepam) – benzodiazepine for
alcohol withdrawal, sedation, sleep. Is
metabolized in the liver – use cautiously.
Nursing Diagnoses Cirrhosis






Fluid Volume deficit
Ineffective protection: bleeding
Disturbed thought process
Ineffective breathing pattern
Impaired skin integrity
Imbalanced nutrition: less than body
requirements
Cirrhosis Interventions- Diet
and fluids





Low protein (sometimes), high carbohydrate, high
calorie-if signs of acute hepatic encephalopathy
With cirrhosis and no hepatic encephalopathy, high
carbohydrate, high protein, low salt
Low sodium-500 mg-2gms
At first sign of encephalopathy or ammonia level
increasing- decrease protein intake (sometimes)
Early stage for liver regeneration- need high
protein-(75-100gms)
Later Manifestations of Cirrhosis
Jaundice
 Jaundice
occurs as a result of the
decreased ability to conjugate and
excrete bilirubin
 In
the late stages of cirrhosis,
patient is usually jaundiced
JAUNDICE
 Hepatocellular
 Obstructive
 Hemolytic
Cirrhosis
Hepatocellular or intrahepatic
jaundice
 Diseased
liver cells can’t clear
normal amounts of bilirubin
from the blood.
Obstructive or Extrahepatic
Jaundice
 Due
to the interference with
the flow of bile in the hepatic
duct.
 Liver is conjugating bilirubin
but it cannot reach small
intestines so is released into
blood stream
Hemolytic Jaundice

Due to excessive destruction of
RBC’s.
– transfusion reaction
– Faulty hemoglobin – sickle cell
– Autoimmune destruction of RBC’s
Major Complications of Cirrhosis
Portal hypertension
Variceal bleeding
Ascites
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
A client is admitted with increased
ascites related to cirrhosis. What is the
priority nursing diagnosis?
n:
...
...
la
n
Im
ba
tiv
e
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d
br
ea
flu
ef
fe
c
In
nu
tr
iti
o
vo
id
th
in
g
lu
m
e
ue
tig
iv
e
ss
4.
Fa
3.
ce
2.
Fatigue
Excessive fluid
volume
Ineffective breathing
pattern
Imbalanced
nutrition: less than
body requirements
Ex
1.
25% 25% 25% 25%
Break!
Portal Hypertension
• The portal vein carries about 1500 ml/min of blood from the
small and large bowel, spleen, and stomach to the liver. Any
obstruction or increased resistance to flow or, rarely,
pathological increases in portal blood flow may lead to portal
hypertension with portal pressures over 12 mm Hg.
• Although the differential diagnosis is extensive, alcoholic
and viral cirrhosis are the leading causes of portal
hypertension in Western countries. Portal vein
thrombosis is the most common cause in children.
Portal Hypertention (Cont’d)
– Increases in portal pressure cause development of a
portosystemic collateral circulation with resultant
compensatory portosystemic shunting and disturbed
intrahepatic circulation.
– These factors are partly responsible for the important
complications of chronic liver disease, including variceal
bleeding, hepatic encephalopathy, ascites, hepatorenal
syndrome, recurrent infection, and abnormalities in
coagulation.
– Variceal bleeding is the most serious complication
and is an important cause of death in patients with
cirrhotic liver disease.
PORTAL HYPERTENSION
normal 3 mmHg
12 mmHg = esophageal rupture

Resistance to blood flow = Increase in pressure
in portal venous system.
– Swelling, inflammation, fibrosis, scarring of liver
– Thrombus
– Resistance in Inferior vena cava: Rt.CHF, myopathy



Blood takes collateral channels - esophagus,
stomach, spleen etc, veins, hemorrhoids
May need shunts or TIPS Transjugular Intrahepatic
Portosystemic Shunt to decrease pressure, beta
blockers also help
TIPS!- You tube
Portal Hypertension
Esophageal
Varices
Arteriovenous shunting
Hypersplenism
Caput
medusae
Moderate anemia
(dilated abd.
veins)
Thrombocytopenia
Hemorrhoids
Neutropenia
Marked ascites
Ascites
Caput medusae
Spider angiomas
Varices
•In Western countries variceal bleeding accounts for about
7% of episodes of gastrointestinal bleeding, although this
varies according to the prevalence of alcohol related liver
disease (11% in the United States, 5% in the United
Kingdom).
• Patients with varices have a 30% lifetime risk of bleeding,
and a third of those who bleed will die. Patients who have
bled once from esophageal varices have a 70% chance of
bleeding again, and about a third of further bleeding
episodes are fatal.
• Several important considerations influence choice of
treatment and prognosis. These include the natural course
of the disease causing portal hypertension, location of the
bleeding varices, residual hepatic function, presence of
associated systemic disease, continuing drug or alcohol
misuse, and response to specific treatment.
Treatment of esophageal
varices
Active bleeding
 Central line & pulmonary artery pressures
 Blood transfusions & fresh frozen plasma for clotting
factors
 Somatostatin or Vasopressin – constrict gut vessels
 Nitroglycerin- to counter negative affects of vasopressin
 Airway/trach
Later prevention of re-bleeding
 Beta-blockers
 Long-acting nitrates
 Soft food, chew well, avoid intra-abdominal pressure
 Protonix (pantoprazole)
Emergency endoscopy
Emergency diagnostic fibreoptic endoscopy is essential to confirm that esophageal
varices are present and are the source of bleeding.
Most patients will have stopped bleeding spontaneously before endoscopy (60% of
bleeds) or after drug treatment.
Endotracheal intubation may be necessary during endoscopy, especially in patients
who are bleeding heavily, encephalopathic, or unstable despite vigorous
resuscitation. In 80% of patients variceal bleeding originates from esophageal varices.
These are treated by injection with sclerosant or by banding.
Sclerotherapy
In sclerotherapy a sclerosant solution (ethanolamine oleate or sodium tetradecyl
sulphate) is injected into the bleeding varix or the overlying submucosa. Injection into
the varix obliterates the lumen by thrombosis whereas injection into the submucosa
produces inflammation followed by fibrosis. The first injection controls bleeding in 80% of
cases. If bleeding recurs, the injection is repeated. Complications are related to toxicity
of the sclerosant and include transient fever, dysphagia and chest pain, ulceration,
stricture, and (rarely) perforation.
Band ligation
Band ligation is achieved by a banding device attached to the tip of the
endoscope. The varix is aspirated into the banding chamber, and a trip
wire dislodges a rubber band carried on the banding chamber, ligating the
entrapped varix. One to three bands are applied to each varix, resulting in
thrombosis. Band ligation eradicates esophageal varices with fewer
treatment sessions and complications than sclerotherapy.
You Tube Band Ligation
Balloon tube tamponade
The balloon tube tamponade may be life saving in patients with active variceal
bleeding if emergency sclerotherapy or banding is unavailable or not technically
possible because visibility is obscured. In patients with active bleeding, an
endotracheal tube should be inserted to protect the airway before attempting to place
the esophageal balloon tube. The Minnesota balloon tube has four lumens, one for
gastric aspiration, two to inflate the gastric and esophageal balloons, and one above
the esophageal balloon for suction of secretions to prevent aspiration. The tube is
inserted through the mouth, and correct placement within the stomach is checked by
auscultation while injecting air through the gastric lumen. The gastric balloon is then
inflated with 200 ml of air. Once fully inflated, the gastric balloon is pulled up against
the esophagogastric junction, compressing the submucosal varices. The tension is
maintained by strapping a split tennis ball to the tube at the patient's mouth.
The esophageal balloon is rarely required. The main complications are gastric and
esophageal ulceration, aspiration pneumonia, and esophageal perforation.
Continued bleeding during balloon tamponade indicates an incorrectly positioned tube
or bleeding from another source. After resuscitation, and within 12 hours, the tube is
removed and endoscopic treatment repeated.
Minnesota balloon for tamponade of esophageal varices
Minnesota
Tube
SengstakenBlakemore tube
– has only 3
lumens
**Respiratory
assessment**
Sengstaken-Blakemore tube – has only 3 lumens
Question:
A)
There is a risk of damage to the oesophageal mucosa from an
inflated oesophageal balloon. Many centres have policies for
routinely deflating and then reinflating the oesophageal balloon. This
varies from 5 minutes deflation every hour to 30-60 minutes every 8
hours. There appears to be little consensus at this time. If the
oesophageal balloon needs to be inflated what is the most accurate
general principle?
The balloon should be deflated and the reinflated every hour.
B)
The balloon should be deflated and then reinflated every 8 hours.
C)
The balloon should never be routinely deflated as the risk of
rebleeding is too great.
D)
The Balloon should be inflated for the absolutely minimum time
necessary.
Long term management of esophageal varices
After acute variceal hemorrhage – prevent rebleeding, which occurs in many patients.
Repeated endoscopic treatment
Repeated endoscopic treatment eradicates esophageal varices in most patients,
recurrent variceal bleeding is uncommon.
Because portal hypertension persists, patients at risk for recurrent varices
Long term drug treatment
The use of beta-blockers after variceal bleeding has been shown to reduce portal
blood pressures and lower the risk of further variceal bleeding. All patients should
take beta blockers unless they have contraindications. Best results are obtained when
portal blood pressure is reduced by more than 20% of baseline or to below 12 mm Hg.
Prophylactic management
Most patients with portal hypertension never bleed, and it is difficult to predict who will.
Beta blockers have been shown to reduce the risk of bleeding.
Transjugular Intrahepatic
Portosystemic Shunt
Special procedures – fistula created with
portal vein and hepatic vein and then stents
placed to keep it open.
 Bypasses the liver by returning blood to
hepatic vein to inferior vena cava
 reduces portal venous pressures and thus
controls bleeding and increases urine output
by inc. venous return
 YouTube- TIPS

TIPS
Transjugular intrahepatic
portosystemic shunt
TIPS POST
*Shunted blood contains
high ammonia
Which can lead to:
hepatic encephalopathy*
Splenomegaly due to
Portal hypertension




The spleen enlarges as blood is
shunted to splenic vein
This increases rate of destruction of
RBCs, WBCs, and platelets
Decreases storage capacity of spleen
Causes anemia, leukopenia and
thrombocytopenia
Ascites – Complication of
Cirrhosis





Blood flow diverted to mesenteric vessels
– Increased capillary pressure leads to fluid
leaving vessels out into peritoneal cavity
High pressure in liver causes fluid to leave liver into
peritoneal cavity
This fluid is plasma filtrate with high concentration
of albumin
Minerals- Ca++ is attached to albumin decreases so
phosphorus increases.
K+ is low due to aldosterone
Four Factors Lead to Ascites
Hypoproteinemia
Increased Na+
&
Increased
capillary
permeability
H2O retention
Portal Hypertension
Responses to third
spacing



Loss of albumin to ascites leads to
hypoproteinemia, depletion of plasma proteins
Loss of blood volume = lowered BP
Reflexes aimed at returning blood pressure to
normal include release of aldosterone
– Increases reabsorption of NA+ back into blood
and H2O follows, thus increasing blood volume
ASCITES
accumulation of high protein fluid in
the abdomen - 3rd spacing
Nursing Management ASCITES



Assess for
Respiratory
Distress- Fowler’s
position helps ease
work of breathing
in ascites
Measure Abdominal
Girth
Accurate I&O
MEDICAL TREATMENT

Na+ restriction500 mg –2 gms

Fluids-1500 ml/day

Diuretics-Aldactone

Albumin - NaCl poor

Paracentesis





To treat respiratory distress
Pt will loose 10-30 grams of protein
Pt in sitting position
Empty bladder first
Post--watch for hypotension,
bleeding, shock & infection
Additional Complications
Liver Failure
Liver Failure
Complex syndrome characterized
by impairment of many organs
and body functions
Two conditions:
 Hepatic Encephalopathy
 Hepatorenal Syndrome
Hepatic encephalopathy:
Alteration in neuro status
due to accumulation of ammonia
Build-up of other substances such as
hormones,
GI toxins, drugs also contribute
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
Precipitating Factors – all place
demands on liver








Bleeding esophageal varices
Ingestion of narcotics or barbiturates,
anesthetics
Excessive protein intake
Electrolyte imbalance
Hemodynamic alterations
Diuretics
Severe infection
Blood transfusions
Stages of Hepatic
Encephalopathy
Hepatic Encephalopathy - Onset Phase

Personality
changes,
disturbances of
awareness,
forgetfulness,
irritability, &
confusion
Hepatic Encephalopathy - Second Phase


Hyperreflexia
Asterixis or flapping
– Altered hand writing

Violent, abusive
behavior
Hepatic Encephalopathy



+ Babinski
hyperactive reflexes
obtained with reflex
hammer
Babinski Video
- Coma
With the
first sign
of hepatic
encephalopathy
decrease
protein intake!
Medical Management
Hepatic Encephalopathy

Neomycin -- intestinal antiseptic-decrease
bacteria that produce ammonia but may
cause renal toxicity or hearing impairment
Lactulose
Converts to lactic and acetic acids
Acid environment decreases
bacterial growth
Increased acidity in the gut converts
ammonia to ammonium ion which
is excreted in feces thus decreases
amount of ammonia available for reabsorption into the blood.
Laxative effect removes ammonia
from bowel. Goal-2-3 loose
stools/day
Give diluted with fruit juice or watervery sweet! Avoid giving with meals.
Hepatic Encephalopathy - Protein
Intake





Decrease protein intake
0-40 grams/day- meat
protein most toxic
Add 10-20 grams every 35 days to max 60gms
If tube feeding use
Hepatic-aid. (reduce
ammonia from protein)
Increase
carbohydrates
Decrease fats
A client with cirrhosis is receiving lactulose to prevent hepatic
encephalopathy. What should the nurse monitor to evaluate
the effectiveness of this medication?
n
A
lir
ub
i
LT
ve
l
le
ve
l
U
nc
on
j
ru
m
ug
a
te
d
am
m
on
bi
ia
le
m
in
Se
4.
al
bu
3.
25% 25% 25% 25%
ru
m
2.
Serum albumin level
Serum ammonia
level
ALT
Unconjugated
bilirubin
Se
1.
A trained nurse can insert a
Sengstaken- Blakemore tube.
50%
ls
e
50%
Fa
2.
True
False
Tr
ue
1.
A client with acute liver failure exhibits confusion, a
declinning level of consciousness, and slowed respirations.
The nurse finds him very difficult to arouse. The diagnostic
information which best explains the clint's behavior is:
em
ia
an
d
i..
.
ia
H
yp
er
gl
yc
cy
to
ro
m
bo
an
Th
m
ia
yc
e
og
l
yp
H
pe
n
i..
.
d
ym
nz
re
liv
e
4.
te
d
3.
ev
a
2.
Elevated liver
enzymes and low
serum protein
Hypoglycemia and
increased serum
ammonia
Thrombocytopenia
Hyperglycemia and
increased creatinine
El
1.
..
25% 25% 25% 25%
Hepatorenal syndrome
Complication of Hepatic
Failure
Hepatorenal syndrome
Complication of Hepatic Failure




kidneys may appear normal
physically but functioning
impaired.
Usually sudden decrease
Urine production,
increase BUN &
Creatinine, jaundice and
signs of liver failure
Poor prognosis- most die
within 3 wks without
transplant
Think due to decreased
perfusion &/or toxins
from failure of liver
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.
Video- What being a donor doesn't mean...


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 for brain dead donor
Liver Transplant Video

Liver transplant
complications





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.
Infection
Most infections can be treated successfully as they
occur.
Cancer
Review
1. Pathophysiology
1. Cirrhosis
2. Portal hypertension
3. Liver failure
1. Encephalopathy
2. Hepato-renal syndrome
2. Signs & Symptoms
3. Treatment
4. Nsg. Care
5. Complications
The End