Download Hepatitis - Austin Community College

Liver Disorders
Part 1
Charlene Morris, RN, MSN
Austin Community College
addenda - D. Bosworth, RN, MSN
A and P Review
Largest organ-weighs 3
lbs
End stage liver diseaseweighs less than 1kg








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

Hepatic artery – 500cc/min oxygenated blood.


30% of Cardiac output goes to the liver
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

Both empty into capillaries/sinusoids
Liver filters the blood

Hepatic vein to inferior vena cava

Lobule –
Functional unit of the liver
Capillaries
Liver section from an animal that has been
injected intravenously with an iron compound.
This material has subsequently been
phagocytosed by the Kupffer cells which line the
sinusoids. Kupffer cells remove bacteria and
toxins form the blood.
The iron has been demonstrated by the Prussion
blue reaction section counterstained with
hematoxylin and Van Gieson .
Note the extensive cytoplasm of the Kupffer cells
in sharp contrast to the small dark nucleus which
is visible when purely morphological stains are
used.
Metabolic Functions of the liver

“Body’s Refinery” Over 400 functions

Primary role in anabolism and catabolism
Metabolic Functions of the Liver
1. Metabolism of Glucose - glucose buffer

When glucose levels rise


liver stores it as glycogen
When glucose levels low



Liver breaks glycogen to usable glucose
Amino acids to glucose
Fatty acids/triglycerides into glucose
Glucagon vs. Insulin
2. Protein – major storage center for protein



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.
3.
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 – release oxygen free
radicals/electrons – vessel & cell damage
HDL caries cholesterol from cells back to the liver
Other functions
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

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
most enters bile the rest enters the blood
Formation and secretion of bile





Contains cholesterol and bile salts to for Digestion of fats.
Fat soluble vitamins absorption
Bile transports Bilirubin to the bowel to be excreted
Some in the stool
In bowel bacteria convert conj. bilirubin to urobilinogen
Urobilinogen reabsorbed into blood and excreted by kidneys
Other transformation processes



Steroids and hormones - acts on these to make
water soluble for excretion – otherwise would
concentrate in body tissues
Ammonia – neuro toxic byproduct of protein
breakdown transformed into urea for excretion
in urine
Drugs, alcohol and toxins metabolism–
transforms to water soluble for excretion
What do these celebrities have in common?
Hepatitis


Inflammation of the liver
Viral hepatitis

Most common cause
Hepatitis

Types of infectious viral hepatitis
A
 B
 C
 D
 E
 G

Hepatitis

Other possible causes
Drugs (alcohol)
 Chemicals
 Autoimmune liver disease
 Bacteria (rarely)

Hepatitis


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

Nearly 400 million people infected with
Hepatitis B


50% to 75% active vial replication
73,000 new cases of Hepatitis B annually in
United States

Incidence decreased due to HBV vaccine
Hepatitis


Approximately 170 million people are infected
with the hepatitis C virus (HCV)
Estimated 30,000 new cases diagnosed annually
Hepatitis


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
Etiology

Causes
A, B, C, D, E, and G virus
 Cytomegalovirus
 Epstein-Barr virus
 Herpes virus
 Coxsackievirus
 Rubella virus

Hepatitis A
Etiology

Hepatitis A virus (HAV)
RNA virus
 Transmitted fecal–oral route, parenteral (rarely)
 Frequently occurs in small outbreaks

Hepatitis A
Etiology

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





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

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

Hepatitis A
Etiology

Hepatitis A virus (HAV)

Anti-HAV immunoglobulin G (IgG)
IgG anti-HAV: Indicator of past infection
 Presence of IgG antibody provides lifelong immunity

Mode of Transmission HAV

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


Occurs more frequently in underdeveloped
countries
Contaminated waters
 Drinking

water, contaminated seafood
Food-borne Hepatitis A outbreaks usually due
to infected food handler
 Contamination
preparation
of food during
Hepatitis A Vaccine
2
doses IM
Initial dose
Booster in 6 to 12 months
Post-exposure Prophylaxis
 Standard
IG-immune globulin
 Given IM within 2 weeks of
exposure
 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
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
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

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
 Kissing/sharing food items may
spread the virus via saliva
 More infectious than HIV
Hep B Incubation Period
 6-24
weeks
 Prevention
Vaccine-3
Initial
doses
dose
Dose at 4 weeks
Dose 5 months later
Post-exposure Hep B
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
 Can give HBV vaccine concurrently

Hepatitis B
Etiology

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

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
Etiology

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 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
 Hepatitis
D virus (HDV) (cont’d)
 HBV-HDV co-infection
 ↑ Risk of fulminant hepatitis
More severe acute disease
Hepatitis E
Etiology

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

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
G virus (HGV) (cont’d)
Coexists with other hepatitis
viruses and HIV
Does not appear to cause liver
damage
Pathophysiology of Hepatitis
 Acute
infection
 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

Flu-like symptoms
 General malaise
 Fatigue
 Body aches, headache
 GI symptoms- nausea/vomiting,
diarrhea, abdominal discomfort
 Chills, low grade fever
Icteric or Jaundice Phase





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
 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

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
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
Hepatitis C
Diagnostic Studies
Anti-HCV
antibody
HCV RNA
Diagnostic tests

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 – liver cancer marker
 Lactic dehydrogenase LDH5 specific for liver
damage

Diagnostic tests





Coagulation – prolonged prothrombin time
due to poor production of clotting factors PT
or INR
Hyponatremia –hemodilution
Hypokalemia, hypophosphatemia,
hypomagnesemia –malnutrition & renal loss
Bilirubin – Total (2-14 umol/L)
Bilurubin – direct/conjugated (0-4 umol/L)
Diagnostic tests
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








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
phenybutazone (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
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.
•Use for patients with blood-clotting problems or excess
fluid
Liver Biopsy









Adequacy of clotting- PT/ INR, Platelets (Vit. K?)
Type and cross match for blood
Stop aspirin, ibuprofen, and anticoagulants 1 wk. before
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
Complications are:
Puncture of lung or gallbladder, infection, bleeding, and pain.
After Needle Liver Biopsy








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.
Soreness at the incision site
Tylenol is used for pain avoid aspirin or ibuprofen for the
first week because they decrease blood clotting, which is
crucial for healing.
Avoid coughing, straining, lifting x 1-2 weeks
Hepatitis Care
 Rest
 Diet
–High calorie & protein, Low fat
 Vitamin supplement – B complex &
K
 Avoid alcohol & drugs detoxed in
liver
 Life style changes
Meds for Chronic Hepatitis

Chronic HBV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Lamivudine (Epivir)
 Adefovir (Hepsera)
 Entecavir (Baraclude)
 Telbivudine (Tyzeka)


Chronic HCV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Rbavirin (Rebetol, Copegus)

Hepatitis
Nursing Management
Nursing assessment
 Past health history
Hemophilia
 Exposure to infected persons
 Ingestion of contaminated food or water
 Past blood transfusion (before 1992)

Hepatitis
Nursing Management
Nursing assessment
 Medications (use and misuse)
Acetaminophen
 Phenytoin
 Halothane
 Methyldopa

Hepatitis
Nursing Management
Nursing assessment
 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

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 and B
Education
Vaccination
Good hygiene practices
Hepatitis
Nursing Management
Nursing implementation
 Health promotion
 Hepatitis C
Education
Infection control precautions
Modification of high-risk behavior
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
 Ambulatory and home care
 Avoid alcohol
 Medication education
α-Interferon administered
subcutaneously
Side effects
Hepatitis
Nursing Management
Evaluation
 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
PSAs
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

Cirrhosis Pathophysiology

Hepatocytes are destroyed and portal
hypertension develops




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 - Laennec’s
 Post necrotic Cirrhosis
 Biliary/obstructive - bile flow
obstructed causing damage to liver
 Cardiac- from right side heart failure
Laennec’s Cirrhosis
Alcoholic or Nutritional 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 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
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
 Salt-poor albumin
 Neomycin – decrease ammonia forming
organisms
 Lactulose – decreases ammonia forming
organisms and inc. acidity of bowel
 Ferrous sulfate and folic acid – to treat
anemia




Beta blocker: propranolol (Inderal) to
prevent bleeding of E varices - in
conjunction with isosorbide mononitrate
(Imdur) lowers hepatic venous pressure
Antacids – 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 , high carbohydrate, high
calorie-if signs of hepatic encephalopathy
 Low sodium-500 mg-2gms
 At first sign of encephalopathy or
ammonia level increasing- decrease protein
intake
 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
PORTAL HYPERTENSION
normal 3 mmHg
now 9-10mmHg
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
Portal Hypertension
Esophageal
Varices
Arteriovenous shunting
Hypersplenism
Caput
medusae
Moderate anemia
(dilated abd.
veins)
Thrombocytopenia
Hemorrhoids
Neutropenia
Marked ascites
Ascites
Caput medusae
Spider angiomas
Rectal varices
Portal hypertension
eventually leads to
esophageal varices.
Portal hypertension-1: varices
The portal vein carries about 1500 ml/min of blood from the small and large bowel,
spleen, and stomach to the liver at a pressure of 5.10 mm Hg. 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, whereas liver disease due to
schistosomiasis is the main cause in other areas of the world. Portal vein thrombosis is
the commonest cause in children.
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.
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
 Airway/trach
Later prevention of re-bleeding
 Beta-blockers
 Long-acting nitrates
 Soft food, chew well, avoid intra-abdominal pressure
 Protonix
Initial measures
Prompt resuscitation and restoration of circulating blood volume is vital and should
precede any diagnostic studies. While their blood is being cross matched, patients
should receive a rapid infusion of 5% dextrose and colloid solution until blood pressure
is restored and urine output is adequate. Saline infusions may aggravate ascites and
must be avoided. Patients who are hemodynamically unstable, elderly, or have
concomitant cardiac or pulmonary disease should be monitored by using a pulmonary
artery catheter, as injudicious administration of crystalloids, combined with
vasoactive drugs, can lead to the rapid onset of edema, ascites, and
hyponatremia. Concentrations of clotting factors are often low, and fresh blood, fresh
frozen plasma, and vitamin K1 (phytomenadione) should be given. Platelet
transfusions may be necessary. Sedatives should be avoided, although haloperidol is
useful in patients with symptoms of alcohol withdrawal.
alcohol withdrawal.
Pharmacological control
Drug treatment, aimed at controlling the acute bleed and facilitating diagnostic
endoscopy and emergency sclerotherapy, may be useful when variceal bleeding is
rapid. Octreotide, a synthetic somatostatin analogue, reduces splanchnic blood flow
when given intravenously as a constant infusion and can be used before endoscopy in
patients with active bleeding. Vasopressin (0.4 units/min), or the long acting synthetic
analogue terlipressin, combined with glyceryl trinitrate administered intravenously or
transdermally through a skin patch is also effective but has more side effects than
octreotide. Glyceryl trinitrate reduces the peripheral vasoconstriction caused by
vasopressin and has an additive effect in lowering portal pressure.
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 90% 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.
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**
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
TIPS
Transjugular intrahepatic portosystemic
shunt
Alternative management Transjugular intrahepatic portosystemic shunt
Transjugular intrahepatic portosystemic shunt is the best procedure for patients
whose bleeding is not controlled by endoscopy. It is effective only in portal
hypertension of hepatic origin. The procedure is performed via the internal jugular
vein under local anesthesia with sedation. The hepatic vein is cannulated and a
tract created through the liver parenchyma from the hepatic to the portal vein,
with a needle under ultrasonographic and fluoroscopic guidance. The tract is
dilated and an expandable metal stent inserted to create an intrahepatic
portosystemic shunt. The success rate is excellent. Hemodynamic effects are
similar to those found with surgical shunts, with a lower procedural morbidity and
mortality. Transjugular intrahepatic portosystemic shunting is an effective salvage
procedure for stopping acute variceal hemorrhage, controlling bleeding from gastric
varices, and congestive gastropathy after failure of medical and endoscopic
treatment. However, because encephalopathy occurs in up to 25% of cases and
up to 50% of shunts may occlude by one year, its primary role is to rescue failed
endoscopy or as a bridge to subsequent liver transplantation.
TIPS POST
cont
**Shunted blood contains
high ammonia
Which will 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
Measure Abdominal
Girth
Accurate I&O
MEDICAL TREATMENT

Na+ restriction500 mg –2 gms

Fluids-1500 ml/day

Diuretics-Aldactone

Albumin - NaCl poor

Paracentesis





Only used if respiratory distress
Pt will loose 10-30 grams of protein
Pt in sitting position
Empty bladder first
Post--watch for hypotension,
bleeding, shock & infection
Review
1. Pathophysiology
1. Cirrhosis
2. Portal hyperetension
3. Liver failure
1. Encephalopathy
2. Hepato-renal
syndrome
2. Signs & Symptoms
3. Treatment
4. Nsg. Care
5. Complications
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


Hyper reflexia
Asterixis or flapping



Altered hand writing
Violent, abusive behavior
EKG changes
Hepatic Encephalopathy


+ Babinski
hyperactive reflexes
obtained with reflex
hammer
- Coma
With the
first sign
of hepatic
encephalopathy
decrease
protein intake!
Medical Management
Hepatic Encephalopathy
Goal is empty sterile bowel

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 3-5
days to max 60gms
If tube feeding use
Hepatic-aid. (reduce
ammonia from protein)
Increase carbohydrates
Decrease fats
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
Liver Transplantation
Only effective treatment for end-stage liver disease.
Offers excellent patient survival and rehabilitation.
Challenges of liver transplantation include a scarcity of human
cadaver donors, rejection, and the limited financial resources
of most patients.
Liver transplantation is a long and complex surgery requiring
surgical expertise in biliary and vascular reconstruction.
Donors:
Live donor liver transplants are an excellent option for some patients.
Liver is the only major organ that will regenerate, both the donor and the recipient
eventually regrow livers of appropriate size for their individual bodies.
Survival rates increase / shorter wait time
Donors to undergo medical and psychosocial testing to rule out any unnecessary
risk
The donor, who may be a blood relative, spouse, or friend, will have extensive
medical and psychological evaluations to ensure the lowest possible risk. Blood
type and body size are critical factors in determining who is an appropriate donor.
Cadaver donor have to wait for brain dead donor
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.
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 complications







Rejection. About 70% of all liver-transplant patients have some
degree of organ rejection prior to discharge.
Antirejection medications are given to ward off the immune
attack.
Infection.
Because antirejection drugs that suppress the immune system.
This problem diminishes as time passes.
Most infections can be treated successfully as they occur.
Cancer
Google Image Result for http://www.hopkinsgi.org/images/shared/disease/database/shared_7441_AD25.jpg
The End