Transcript Nursing Care of Patients with Hepatobiliary Disorders

Nursing Care of Patients with
Hepatobiliary Disorders
C. Cummings RN, EdD.
Anatomy
Diaphragm
Liver
Hepatic
Duct
Cystic
Duct
Gall
Bladder
Common
Bile Duct
Pancreas
Sphincter of
Oddi
Duodenum
Pancreas
• Exocrine- 80% of organ, acinar cells with
digestive enzymes:
– What are they?
• Endocrine- islets of langerhans
– Alpha cells- ?
– Beta cells- ?
Acute Pancreatitis
• Cause:
– Pancreatic enzymes destroy ductal tissue and cancreatic
cells autodigestion and fibrosis
– Can be life threatening
– NHP- necrotizing hemorrhagic pancreatitis
• 20%, diffuse bleeding
– Enzymes are activated before they reach the duodenum
– Toxic injury to pancreatic cells
Four major physiologic processes
• Lipolysis
– Caused by lipase, release fatty acids and combine
with I Ca  causes?
– Proteolysis
– Caused by trypsin, splits proteins into smaller
polypeptides  what??
Four major physiologic processes
• Necrosis of the Blood Vessels
– Caused by elastase, elastic fibers of the blood vessels and
ducts dissolve  what?
– Kallikrein releases vasoactive peptides, bradykinin and
kinin what? and increased ?
• Inflammation
– Leukocytes form around hemorrhagic and necrotic areas
 pus, abcess formation and if walled off pancreatic
what??
Why does enzyme activation occur?
• Bile Reflux- obstruction of CBD
• Hypersecretion-obstruction theory- pancreatic duct
ruptures
• Alcohol induced changes- stimulates hydrochloric
acid and secretin production exocrine functions,
also causes edema of the duodenum and ampulla of
Vater, this obstructs flow, may also decrease tone at
sphincter of Oddi and cause duodenal reflux
Other causes
 Besides alcohol ingestion and biliary
disorders, can also be caused by:
 Trauma- blunt or surgical (whipple/ ERCP)
 Pancreatic obstruction- such as?
 Metabolic disturbances- hyperlipidemia,
hyperparathyroid
 Renal failure or transplant
 Ulcers that lead to peritonitis
 Coxsackievirus B infections
 Drug toxicities- such as?
Complications
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Pancreatic infection
Peritonitis
Hypovolemia
Hemorrhage
ARF
Paralytic ileus
Septic Shock
What are other
complications??
Symptoms of Acute Pancreatitis
• What is predominant
symptom?
• Where is it?
• When is it worse?
• Jaundice
• Cullen’s sign- what is that?
• Turner’s sign- and that?
• Bowel sounds may be
decreased or absent
• Abdominal tenderness
• Watch for signs of shock
• Respiratory effusions/ SOB
• Assess for excessive alcohol
intake
Turner’s sign
Laboratory Diagnoses
• Elevated Serum
– What are major enzymes?
– Trypsin
– Elastase
• Also, increased serum
– Glucose
– Bilirubin
– Alanine aminotransferase
– Leukocyte count
• Decreased
– Calcium and magnesium
Diagnoses for Acute Pancreatitis
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What are two primary nursing diagnoses?
Nausea
Risk for fluid volume deficit
Risk for infection
Risk for ineffective breathing pattern
Risk for activity and sleep disturbances
Collaborative Diagnoses
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What are two potential nursing diagnoses?
Potential for Hypovolemic or Septic Shock
Potential for ARDS
Potential for Paralytic Ileus
Potential for MOSF
Nursing Interventions
• Acute Pain
• What is primary method to
relieve pain, other than
medication?
• IV fluids for hydration
• Replacement of Ca and Mg
• NG drainage and suction
• Assess for return of bowel
sounds and pain control
Pain Control
• Opiods, IV and PCA
• Demerol for relief of spasms
at the sphincter of Oddi, but
it has problems with
breakdown and is rarely
used now
• Fentanyl patch
• Epidural morphine with
bipivacaine
• Pain may last how long?
Other management of pain
• Anticholinergics, atropine, glucagon,
calcitonin, histamine receptor antagonists
(Zantac), protease inhibitors are used for
what?
• Antibiotics
– Ceftazidime, cefuroxime, imipenem (Primaxin)
Other Management of Pain
Surgery
ERCP (endoscopic retrograde
cholangiopancreatography)
- used to open sphincter
Pseudocystojejunostomy or
Pseudocystogastrotomy to drain abcess or
pseudocyst
JP drains or sump tubes may be used for excessive
drainage
ERCP
ERCP
Imbalanced nutrition: less than body
requirements
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Maintain on NPO, may have NGT
May not eat for 7-10 days
Receive nutritional support through what?
Begin back on what kind of diet? What should
they not take in?
• Diet teaching and teaching on signs of chronic
progression should be stressed with the
patient
Chronic Pancreatitis
• Usually develops after repeated episodes of acute
pancreatitis
• What is the most common cause?
• Types:
– Chronic Calcifying Pancreatitis- alcohol induced,
proteins plug the ducts 
– lead to atrophy and dilation 
– ulceration and inflammation 
– fibrosis, intraductal calification and cystic sacs
develop
– Hard, firm organ with pancreatic insufficiency
Chronic Pancreatitis
• Type
– Chronic Obstructive Pancreatitis
• Inflammation, spasm and obstruction of the sphincter
of Oddi
• Inflammation and sclerotic lesions occur at the head of
the pancreas obstruction and backflow of secretion
Chronic Pancreatitis with pseudocysts
Results
• Loss of exocrine function:
– Aqueous bicarbonate- neutralizes duodenal
contents
– Pancreatic enzymes- what do they do?
– Enzyme secretion is reduced by 80% 
steatorrhea, what do the stools look like?
– Fat malabsorption  wt loss and muscle wasting
and edema r/t loss of albumin
Results
• Pancreatic endocrine dysfunction causes what
disease?
• May also have pulmonary complications from
edema and pancreatic ascites
• ARDS may develop
• Chronic pancreatitis is a major risk factor for
pancreatic cancer
Symptoms of Chronic Pancreatitis
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Intense abdominal pain and tenderness
Ascites
What type of stools?
Respiratory compromise
Wt loss or gain?
Jaundice
What does the urine look like? Why?
Signs of diabetes
Elevated lipase and amylase
Elevated bilirubin, alkaline phosphatase and glucose
Definitive dx- by biopsy to look for calcification
Nursing Management
• Manage pain- how?
• Enzyme replacement- dietary supplements,
pancrease, viokase, cotazyme, donnazyme- take
before or during meals, take according to number of
stools/day and wipe lips after
• Insulin therapy
• NPO or TPN for days, then what kind of diet?
• Histamine receptor blockers to decrease acid
• Octreotide (Sandostatin) like somatostatin may be
used for diarrhea to slow motility
Health teaching
• Surgery is not an option, unless there is a cyst,
obstruction or possible transplant for diabetes
• Diet and alcohol avoidance is stressed
• Medication compliance with insulin,
pancreatic enzymes
• Skin care for irritation r/t steatorrhea
• What should the patient monitor?
Case Study
• 44 year old female
admitted with
abdominal pain, nausea
and vomiting. She
states that she has a lot
of gas pain that wakes
her up in the night.
• What do you suspect?
Case Study
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What are the symptoms of GB disease?
What can precipitate it?
What is the treatment?
How can you prepare her for surgery? How do
you decide between laparoscopic and open?
• What needs to be done postop?
Case Study
• What structures are located in the RUQ of the
abdomen?
• Which of the above organs are palpable in the
RUQ?
• Given the patient’s diagnosis, what lab values
would be important to evaluate?
• List 4 preop preparations that to be done.
Case Study
• The patient undergoes a laproscopic
cholecystectomy, why is a T-tube inserted?
• What type of postoperative care would be
required?
• The patient is sent home with the T-tube,
what care would be appropriate?
• What type of diet should they be on?
Case Study
• The patient is medicated with Morphine and the pain
has decreased from 10-4 in 1 hour, what else could
be done for his pain?
• What data charted in the assessment is consistent
with common bile duct obstruction?
• The patient spikes a temp of 38.6, a CXR is ordered
and the patient is started on an antibiotic, imipenem.
What should be done before the antibiotic is
started?
Case Study
• She is ready for
discharge
• What type of teaching is
needed?
• What should be
avoided, what about
care of the T-tube?
Cholecystectomy
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Removal of the Gallbladder
Can be done open or laproscopic
Signs are nausea, vomiting, abdominal pain
Risk Factors:
– Fat, Female, Forty and Fertile
– lap cholecystectomy
Lap Cholecystectomy
T-tube
Post-operative Care
• Pain control- demerol or PCA
• NPO until bowel sounds return, then clear
liquids to DAT
• Diet depends on what patient can tolerate
• T-tube may remain in for 1-6 weeks
– Monitor drainage, should be bile colored
– Less than 1000ml/day
– Never irrigate, aspirate or clamp a T-tube without
an MD order
Disorders of the Liver
• Largest organ in the body
and is located in the RUQ
• Large right lobe and smaller
left lobe
• Made up of lobules
• Bile is made in hepatocytes,
secreted into bile canaliculi
• Receives 1500 ml of
blood/min
Liver Functions
 400 functions
 Storage:
 What types of vitamins and
minerals?
 Protective:
 Kupfer cells, phagocytic,
destroy bacteria, anemic
RBC’s
 Detoxifies what?
 Metabolism:
 Makes proteins, for
what?
 Breaks down amino acids
to remove ammonia,
converted to what?
 Synthesizes plasma
proteins, albumin,
prothrombin and
fibrinogen
 Stores and releases
glycogen
 Breaks down and stores
fatty acids and
triglycerides
 Forms and secretes what
substance?
Liver Disorders
• Cirrhosis/ Liver
Failure
• Hepatitis
Case Study
53 year old male admitted
to the ED with
abdominal pain, nausea
and vomiting, weight
loss. His abdomen is
large and tender. His
skin is light yellow. He
has a fruity odor to his
breath.
What do you suspect?
Case Study
• What lab work should be done?
• What interventions would you perform and
why?
• Your patient becomes belligerent after a few
hours and wants to leave, what would you do?
• What radiology studies may be done?
Case Study
• His liver enzymes are extremely elevated and
he is becoming confused. He is admitted to
the floor.
• What symptoms are you likely to see in this
patient?
• He starts to vomit blood, what does this mean
and what may be done?
• What medications may be given to this
patient?
Case Study
• He has improved and is
now ready for
discharge.
• What kind of teaching
would this patient
need?
• What should be done
about rehab?
Cirrhosis
• Scarring of the liver, caused by a chronic, irreversible
reaction to hepatic inflammation and necrosis
• Causes:
– #1 cause?
– #2 cause?
• Destruction of hepatocytes, tissue becomes nodular,
block bile ducts and blood flow from fibrous
connective tissue
• Liver begins enlarged and then shrinks
Cirrhosis
Complications
• Compensated and Decompensated Cirrhosis
• Liver failure 
– Portal hypertension, what is this?
– Ascites, why?
– Bleeding esophageal varices
– Coagulation defects, why?
– Jaundice, what causes this?
– Portal systemic encephalopathy and coma
– Hepatorenal syndrome
– Bacterial peritonitis
Liver Dysfunction
PSE
Esophageal Varices
Jaundice
Bleeding
Hepatorenal
Syndrome
Bacterial
Peritonitis
Ascites
Portal Hypertension
• Increase in pressure within the portal vein
• Increased resistance or blockage in the flow of blood
through the portal vein
• Seeks collateral circulation
• Blood flows back into the spleen, causing
splenomegaly
• What veins become dilated?
• Can lead to esphageal varices, caput medusa (what is
that??) and hemorroids
Ascites
• Accumulation of free fluid within the peritoneal cavity
• Increased hydrostatic pressure from the portal hypertension
causes fluid to leak into cavity
• Albumin accumulates in peritoneal fluid and this reduces the
circulating proteins, this decreases serum colloid osmotic
pressure and can lead to a decrease in what?
• Decrease in intravascular circulation causes renal
vasoconstriction, triggers the renin-angiotensin system. This
causes Na and water retention, which does what to fluid
hydrostatic pressure and fluid volume?, where does the fluid
accumulate?
Ascites
Bleeding esophageal varices
• Blood backs up from liver into esophageal and gastric
vessels
• Increased pressure, causes esophageal vessels to become
fragile and distended
• Life threatening emergency, significant blood loss and this
can lead to what?
• Bleeding is manifested as hematemesis and melena, what
does that mean?
• Any activity that increases abdominal pressure can lead to
bleeding, such as what?
• Also, then to have portal hypertensive gastropathy, this
leads to slow GI bleeds and cause chronic anemia
Coagulation defects
• Decrease in the synthesis of bile, this prevents the
absorption of fat-soluble vitamins and clotting
factors are not produced
• What fat soluble vitamin is predominant in clotting?
• What lab values would be abnormal?
• Splenomegaly results from the backup of blood, this
destroys platelets and leads to thrombocytopenia,
one of earliest signs of liver dysfunction
Jaundice
• Hepatocellular disease and intrahepatic obstruction
are the cause
• Liver cells can not excrete bilirubin, what are the liver
cells called?
• Excessive circulating bilirubin
• Obstruction jaundice is from edema, fibrosis and
scarring that block bile ducts
• Excess bilirubin causes the skin to become yellow
gold, sclera are yellow and skin is pruritic and
“frosty”
Portal system encephalopathy
• PSE or hepatic coma in later stages
• Altered level of consciousness, impaired thinking and
neuromuscular disorders
• Can reverse the encephalopathy with early
intervention
• Liver is unable to detoxify substances and ammonia
is most common cause
• Some encephalopathy may occur without elevated
ammonia, may be other toxins
Portal systemic encephalopathy
 Factors that may precipitate:
 High-protein diet
 Infections
 Hypovolemia
 Hypokalemia
 Constipation
 GI bleeding, large protein load in intestines
 Drugs, such as hypnotics, opioids, sedatives, analgesics
and diuretics
 Paracentesis or shunting of veins may also cause
 Why does protein increase encephalopathy??
Stages of encephalopathy
• Prodromal
– Personality changes, agitation, emotional lability, impaired
thinking, fatigue, slurred speech, inability to concentrate
• Impending
– Mental confusion, disoriented to person, place and time,
asterixis (liver flap) how do you test for this?
• Stuporous
– Drowsy, but arousable, muscle twitching, hyperreflexia,
abnormal EEG
• Comatose
– Unresponsive, 85% lead to death, obtunded, response to
pain, no asterixis, positive babinski, muscle rigidity, fetor
hepaticus, seizures, why seizures?
Hepatorenal syndrome
• Often cause of death
• Sudden decrease in urinary flow
• Elevated BUN and Creatinine levels and
decreased urine sodium excretion
• Increased urine osmolarity, what is that?
• Why is there a decrease in fluid volume to the
kidneys?
Bacterial Peritonitis
• Occurs spontaneously
• Low concentrations of what type of proteins, that
protect against bacteria, cause this?
• Bacteria are from the bowel and reach the ascitic
fluid when they are pulled through the bowel
wall, what type of pressure would cause this?
• Symptoms are: fever, chills, abdominal pain and
tenderness
• Diagnosis is made by culture of ascitic fluid and
leukocyte count
Causes of Cirrhosis
• Alcoholic hepatitis- if alcohol intake is stopped, liver
damage will reverse, if not, cellular necrosis continues. It
may take years to develop
• Viral Hepatitis- C is most common, but B may also affect.
It causes inflammation and cell damage
• Autoimmune hepatitis- autoantibodies
• Steatohepatitis- “fatty liver” fat and cholesterol deposits
occur over time, cause is obesity and elevated lipids
• Drugs and toxins- medications, such as illegal drug use,
chemotherapy, tylenol !
• Biliary disease- primary biliary cirrhosis and primary
sclerosing cholangitis
• Metabolic- hematochromatosis, what is that?, Alphaantitrypsin deficiency and cystic fibrosis, why?
Cirrhosis Patient
Physical Manifestations
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Fatigue
Change in wt
GI symptoms
Abdominal pain and
tenderness
Pruritis
Jaundice and icterus (what’s
that?)
Dry skin and rashes
Petechiae and ecchymosis,
why?
Vascular lesions, “spider
angiomas” on nose, checks,
shoulders
Dependent edema
Physical manifestations
• Ascites, can lead to disruption in what major
function?
• Tested by fluid wave, what is that?
• How do you test for hepatomegaly?
• Why would you measure abdominal girth?
• Melena and fetor hepaticus may also be present,
what does this mean?
• Amenorrhea, testicular atrophy and gynecomastia
may also occur because of inactive hormones that
are normally made in the liver
Fluid Wave
Lab tests
 Elevated values are:
 AST
 ALT
 LDH
 Alkaline phosphatase
 Bilirubin in serum and
urine
 Total protein
 Serum globulin
(immune response to
liver disease)
 Ammonia
 Prothrombin time
 Decreased values are:
 Fecal urobilinogen
 Total protein (in chronic
disease)
 Serum albumin
Other assessments
• CT scan, Ultrasound of liver
• Liver Biopsy, how is this done and what
precautions should be taken?
• EGD- what does this mean and why would this
be done, what are they looking for?
Liver Biopsy
Nursing Diagnoses
• #1 is related to fluid volume, would it be
excess or deficit fluid volume, what is it
related to?
• What are two potential problems?
• What collaborative problems are these
patients at risk for? (there are at least 7 or 8)
Nursing Management of Excess Fluid
Volume
• Diet Therapy
– Low Na diet, 500 to 2 gm/day
– IV and oral fluid is restricted to 1-1.5 L/day
– Vitamin supplements, thiamine, folate may be needed
• Drug Therapy
– Diuretics, what are some?
– What should you monitor for?
– What electrolyte is affected by diuretics?
– Antibiotics to prevent bacterial peritonitis
Management of Excess Fluid Volume
• Paracentesis
– MD inserts a catheter into the abdomen to
remove and drain ascitic fluid
– Should void first, HOB is elevated
– Should monitor vital signs and drain slowly, why?
– Cultures may be sent
– What blood product may be given prior to
removing ascites fluid?
Paracentesis
Other measures
• Comfort:
– Keep HOB elevated, use creams for pruritis
– Monitor lung sounds and give O2 if needed
– Monitor fluid and electrolyte levels
• Surgical:
– Peritoneovenous shunt- catheter and one way valve to let fluid
flow from abdomen to superior vena cava, can have clots and
infection
– Portacaval shunt- diverts blood from the liver to the kidney or
inferior vena cava
– TIPS- transjugular intrahepatic portal-systemic shunt, track is
made between the portal vein, hepatic veins and systemic
circulation. The shunts are kept open with stents that are
inserted and this increases the systemic circulation and decreases
the portal hypertension
Peritoneal-venous Shunt
TIPS
Nursing Outcomes for Excess Fluid Volume
• Name 8 desired nursing outcomes for a patient with
excess fluid volume
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• 7.
• 8.
Potential for Hemorrhage
• Goal is to prevent bleeding
• Drug therapy is to control HR and BP, this
decreases the hepatic venous pressure gradient,
may use a Beta Blocker to do both and keep the
HR about 55/min
• Gastric Intubation- NGT with iced saline or water
lavage to vasoconstrict ulcerations
• device.
Potential for Hemorrhage
• Balloon Tamponade- esophagogastric- Blakemore
tube- it has 2 balloons, an esophageal and gastric,
one balloon in esophagus to compress varices, one
larger in stomach to anchor tube, and another lumen
for suctioning. Inserted through the mouth, once in
place, balloons are inflated and clamped. Traction
may be performed by anchoring it to a helmet
Potential for Hemorrhage
• Complications of the Blakemore tube are aspiration, the
balloons may decompress and become lodged in the back
of the pharynx. Blood and gastric contents may also be
aspirated. The stomach balloon should always be deflated
first and then the esophageal.
• Blood transfusions may be needed and emergently, PRBC’s
and FFP
Potential for Hemorrhage
• Endoscopic- Band Ligation- small “O” bands are
placed around the base of the varices, octreotide
may be given at the time to decrease bleeding and
secretions. Injection sclerotherapy may also be done
to stop bleeding, a sclerosing agent is injected via
endoscopy
• TIPS procedure or portal-systemic shunts may be
needed
• What lab work should be monitored for these
patients?
Banded esophageal Varices
Blakemore Tube
Portal Systemic Encephalopathy
• Ammonia is the probably cause, toxic to the brain
• Drug Therapy- Lactulose- high molecular wt disaccharide,
it is thick and sticky with a sweet taste. It cleanses the GI
tract and decreases the bacterial content, also creates and
acid environment in the bowel and decreases the acid
from 7-5, this keeps ammonia as an ion and pulls it into
the colon. It may be given po or enema. Po is 20-30g q 4
hour. Monitor the number of stools and ammonia levels.
It may cause cramping and often patients do not want to
take it.
Portal-Systemic Encephalopathy
• Drug Therapy- Neomycin may also be used to
cleanse the bowel and decrease protein breakdown,
it can be given po or enema. Metronidazole (Flagyl)
is also a bowel antibiotic with less renal side-effects
• Monitor the patient for neurologic changes, look for
stupor, asterixis and fetor hepaticus
• Maintain patient safety
Patient Education
• Patient teaching should revolve around
three main areas, what should be discussed
under each?
• 1. Diet Therapy
• 2. Drug Therapy
• 3. Alcohol Abstinence
• Goal is to have a decrease in ascites,
electrolytes WNL and no bleeding or PSE
Hepatitis
• Viral infection, can be acute or chronic, caused by
one of five viruses, A-E, hepatitis F and G have been
identified too
• Leads to inflammation of the liver cells
• Can also be caused by exposure to chemicals, toxins
and medications
• Can be secondary to infections from Epstein-Barr,
herpes, varicella and cytomegalovirus
Hepatitis
Types of Hepatitis
• Hepatitis A
– HAV is an RNA virus
– Spread fecal-oral, contaminated water, shellfish
and food contaminated by food handlers
– Incubation is 15-50 days
– Often the disease is mild and people don’t know
that they have it
– Can lead to more severe liver disease in
compromised people
Types of Hepatitis
• Hepatitis B
– HBV, it is a particle of DNA that is surrounded by a core and
surface antigen
– Spread by:
• Unprotected sex
• Sharing needles or needle sticks
• Blood transfusions, hemodialysis
• Maternal-fetal route
– Symptoms occur in 25-180 days. They are:
• Anorexia, nausea, vomiting, fever, fatigue, RUQ pain, dark
urine and light stool, joint pain and jaundice
– Can lead to cirrhosis and liver failure
– Often develop immunity and can become carriers
Hepatitis C
• HCV is a single strand RNA virus
• Transmitted blood to blood
• Spread by:
– IV drug needle sharing
– Blood, blood products or transplants
– Needle stick injury with contaminated blood
– Tattoos and intranasal cocaine
• Not transmitted by casual contact
• Should not share razors, toothbrushes or pierced earrings
• Incubation is 21-140 days, average 7 weeks
• Most don’t know they are infected until it becomes chronic
• Scarring leads to cirrhosis, can lead to liver cancer
• Many receive liver transplants
Hepatitis D
• HDV is a defective RNA virus that needs helper
function of HBV
• Coinfects and needs HBV for replication
• Can be a superinfection and lead to a chronic
infection
• Incubation is 14-56 days
• Spread is mostly IV blood transmission
Hepatitis E
• HEV, single strand RNA virus
• Transmitted by fecal-oral route, similar to HAV
• Waterborne epidemic in India, now in Asia,
Africa, Middle East, Mexico and Central &
South America
• Incubation of 15-64 days
Incidence
• 250,000 people in the US develop HAV
• 200 million worldwide have HCV
• 3.9 million have HCV in the US and 3 million have
chronic liver disease
• Chronic hepatitis is through to be inflammation of
the liver for > 6 months
• Usually the result of HCV or HBV
• Can lead to fulminant liver failure, which is lifethreatening, due to total failure of the organ
Prevention
• What things can you tell a client to prevent
the spread of hepatitis? (for both HAV and
HBV/HCV)
• Which viruses have vaccines?
• If exposed to the virus, is there anything that
can be taken?
Patient assessment
• Assess for:
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Abdominal pain
Jaundice
Arthralgia
Myalgia, why?
Diarrhea
Changes in stool and urine
color
– Fever, lethargy
– Nausea/vomiting
– History of contamination
• Liver Biopsy- confirmatory
• Labs:
– Liver enzymes- AST, ALT, alk
phos, bilirubin all elevated
– Enzyme assays- antibodies
to virus, anti-HAV, HBsAG
(HBV surface antigen), anti
HBcIgM (core antigen)
– Elisa for HCV and antiHCV
– Anti-HDV and HEV
– Usually present within 6
months
Nursing Diagnoses
• What do you think are the most common
nursing diagnoses for Hepatitis?
• 1.
• 2.
• 3.
• What interventions would be appropriate?
Nursing Interventions
• Drug Therapy
– Use medications sparingly to rest liver
– Antivirals, such as lamivudine (epivir-HBV) or
Hepsera
– Interferon for HCV and HBV, SQ with ribavirin, take
the combination for 24-48 weeks until negative
HCV RNA level
Home Care Education
• What type of home care education would be appropriate?
– Discuss disease with family, especially spread
– Discuss community resources, chronic, long term disease
– Good handwashing, prevent spread of blood
– Measures to prevent the spread of infection to the patient
– Avoid alcohol
– Allow for rest periods
Liver Transplantation
• Assess patient both physically and psychologically prior to
transplantation
• Contraindicated if:
– Severe cardiovascular or respiratory disease
– Active alcohol or drug use
– Metastatic disease
– Inability to follow treatment or lack of appropriate caregiver
• Most transplants are cadaver livers, but some are donors of single
lobes. Usually done with children
• Livers are obtained through the UNOS, United Network of Organ
Sharing in cooperation with OPO, organ procurement organizations.
In Jacksonville, we use Lifequest. There are presently 2300 people
waiting for organ transplants within our area.
Liver Transplantation
• Most common complications are graft rejection and infection
• Rejection can occur quickly or years out.
• Medications to prevent rejection are:
– Cell-cept, Prograf, Imuran, Sirolimus, prednisone and FK506
• Signs of rejection are RUQ pain, fever, tachycardia, decreased
bile production and increased jaundice, elevated liver
enzymes
Liver Transplantation
 Infection
 Immunosuppressive therapy can cause rejection,
plus they are very debilitated, immobile and have
multiple lines
 Cytomegalovirus, mycobacterial and parasitic
infections are most common
 Usually on many antibiotics
 Other complications:
 Hemorrhage, hepatic artery thrombosis,
pulmonary atelectasis, electrolyte imbalancesusually Ca, Mg and K, ARF
Nursing Care
• Usually these patients are very ill, they may be in the
ICU for many days, some are “fast-tracked”
• Return intubated, with a Swan line, arterial line and
have continuous cardiac outputs and SvO2 readings.
• Some are on CVVH (continuous veno-venous
hemofiltration) for renal perfusion
• Need a lot of psychological support
Liver transplantation
liver transplant
UNOS
Liver transplant video
• http://www.youtube.com/watch?v=If5dIwcGZ
Y0Liver transplant surgery