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Care of Patients with Liver Problems

Chapter 61

Mrs. Kreisel MSN, RN


NU130 Adult Health
Summer 2011

Cirrhosis
Cirrhosis is extensive scarring of the liver, usually
caused by a chronic reaction to hepatic
inflammation and necrosis.
Complications depend on the amount of damage
sustained by the liver.
In compensated cirrhosis, the liver has significant
scarring but performs essential functions without
causing significant symptoms.

Complications

Portal hypertension
Ascites
Bleeding esophageal varices
Coagulation defects
Jaundice
Portal-systemic encephalopathy with hepatic
coma
Hepatorenal syndrome
Spontaneous bacterial peritonitis

Esophageal
Varices

Etiology
Known causes of liver disease include:
Alcohol
Viral hepatitis
Autoimmune hepatitis
Steatohepatitis
Drugs and toxins
Biliary disease
Metabolic/genetic causes
Cardiovascular disease

Clinical Manifestations
In early stages, signs of liver disease include:
Fatigue
Significant change in weight
GI symptoms
Abdominal pain and liver tenderness
Pruritus

Clinical Manifestations (Contd)


In late stages, the signs vary:
Jaundice and icterus (pigmentation of tissue,
membranes and secreations with bile pigments)
Dry skin
Rashes
Petechiae, or ecchymoses (lesions)
Warm, bright red palms of the hands
Spider angiomas: associated with cirrhosis of the liver,
branched growth of dilated capillaries on the skin
looking like a spider
Peripheral dependent edema of the extremities and
sacrum

Abdominal Assessment

Massive ascites
Umbilicus protrusion
Caput medusae (dilated abdominal veins)
Hepatomegaly (liver enlargement)

Liver
Dysfunction

Other Physical Assessments


Assess nasogastric drainage, vomitus, and stool for
presence of blood
Fetor hepaticus (breath odor)
Amenorrhea
Gynecomastia, testicular atrophy, impotence
Bruising, petechiae, enlarged spleen
Neurologic changes
Asterixis ( also known as liver flap or liver tremors:
abnormal involuntary jerking muscles)

Laboratory Assessment
Aminotransferase serum levels and lactate
dehydrogenase may be elevated.
Alkaline phosphatase levels may increase.
Total serum bilirubin and urobilinogen levels may
rise.
Total serum protein and albumin levels decrease.

Laboratory Assessment (Contd)


Prothrombin time is prolonged; platelet count is
low.
Hemoglobin and hematocrit values and white
blood cell count are decreased.
Ammonia levels are elevated.
Serum creatinine level is possibly elevated.

Excess Fluid Volume


Interventions:
Nutrition therapy consists of low sodium diet,
limited fluid intake, vitamin supplements.
Drug therapy includes a diuretic like Lasix,
electrolyte replacement.
Paracentesis is the insertion of a trocar
catheter into the abdomen to remove and
drain ascitic fluid from the peritoneal cavity.
Observe for possibility of impending shock.

Comfort Measures
For dyspnea, elevate the head of the bed at least
30 degrees, or as high as the patient wishes to
help minimize shortness of breath.
Patient is encouraged to sit in a chair.
Weigh patient in standing position, because
supine position can aggravate dyspnea.

Fluid and Electrolyte


Management
Interventions:
Fluid and electrolyte imbalances are common
as a result of the disease or treatment; test for:
Blood urea nitrogen level
Serum protein level, if low may order
albumin (protein)
Hematocrit level
Electrolytes

Surgical Interventions
Peritoneovenous shunt & Portocaval shunt are rarely
done today because of serious complications. They are
shunts that divert fluid away from the diseased liver into
the venous system.

Transjugular intrahepatic portosystemic shunt is a


nonsurgical procedure done in interventional radiology.
Thread a balloon through the jugular to the liver into the
portal vein. Enlarge it with a balloon and insert a stent
to keep it open

Potential for Hemorrhage


Interventions include:
Identifying the source of bleeding and initiating
measures to halt it
Massive esophageal bleeding
Esophageal varices

Potential for Hemorrhage (Contd)


Nonsurgical management includes:
Drug therapypossibly nonselective beta
blocker
Gastric intubation
Esophagogastric balloon tamponade: catheter
surround3d by a balloon used in the
esophagus to arrest bleeding from varices. 3
lumens, one for fluids, one balloon, control of
the balloon

Esophageal
Gastric
Tamponade

Management of Hemorrhage

Blood transfusions
Esophagogastric balloon tamponade
Vasoactive therapy
Endoscopic procedures
Transjugular intrahepatic portal-systemic shunt
Surgical management

Potential for Portal-Systemic Encephalopathy


Interventions include:
Role of ammonia: it is converted into urea in the liver
and along with CO2 it becomes the final product of
protein metabolism
Reduction of ammonia levels High levels indicate
Liver Failure
Nutrition therapy using simple and brief guidelines
Drug therapy:
Lactulose: Empty the bowel of ammonia
Neomycin sulfate
Metronidazole

Hepatitis
Widespread viral inflammation of liver cells
can lead to Hepatic Encephalopathy (brain
dysfunction due to high ammonia levels or
orther liver problems. Can lead to a coma.
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E

Hepatitis A
Similar to that of a typical viral syndrome; often goes
unrecognized
Spread via the fecal-oral route by oral ingestion of fecal
contaminants
Contaminated water, shellfish from contaminated water,
food contaminated by handlers infected with hepatitis A
Also spread by oral-anal sexual activity
Incubation period for hepatitis A is 15 to 50 days.
Disease is usually not life threatening.
Disease may be more severe in individuals older than
40 years.
Many people who have hepatitis A do not know it;
symptoms are similar to a GI illness.

Hepatitis B
Spread is via unprotected sexual intercourse with
an infected partner, sharing needles, accidental
needle sticks, blood transfusions, hemodialysis,
maternal-fetal route.
Symptoms occur in 25 to 180 days after
exposure; symptoms include anorexia, nausea
and vomiting, fever, fatigue, right upper quadrant
pain, dark urine, light stool, joint pain, and
jaundice.
Hepatitis carriers can infect others, even if they
are without symptoms.

Hepatitis C
Spread is by sharing needles, blood, blood
products, or organ transplants (before 1992),
needle stick injury, tattoos, intranasal cocaine
use.
Incubation period is 21 to 140 days.
Most individuals are asymptomatic; damage
occurs over decades.
Hepatitis C is the leading indication for liver
transplantation in the United States.

Hepatitis D
Transmitted primarily by parenteral routes
Incubation period 14 to 56 days

Hepatitis E
Present in endemic areas where waterborne
epidemics occur and in travelers to those areas
Transmitted via fecal-oral route
Resembles hepatitis A
Incubation period 15 to 64 days

Clinical Manifestations

Abdominal pain
Changes in skin or eye color (Jaundice)
Arthralgia (joint pain)
Myalgia (muscle pain)
Diarrhea/constipation
Fever
Lethargy
Malaise
Nausea/vomiting
Pruritus (itching)

Nonsurgical Management

Physical rest
Psychological rest
Diet therapy
Drug therapy includes:
Antiemetics
Antiviral medications
Immunomodulators
AVOID DRUGS METABOLISED BY THE
LIVER SUCH AS TYLENOL

Fatty Liver (Steatohepatitis)


Fatty liver is caused by the accumulation of fats in
and around the hepatic cells.
Causes include:
Diabetes mellitus
Obesity
Elevated lipid profile
Alcohol abuse
Many patients are asymptomatic.

Hepatic Abscess
Liver invaded by bacteria or protozoa causing
abscess
Pyrogenic liver abscess; amebic hepatic abscess
Treatment usually involves:
Drainage with ultrasound guidance
Antibiotic therapy

Liver Trauma
The liver is one of the most common organs to be
injured in patients with abdominal trauma.
Clinical manifestations include abdominal
tenderness, distention, guarding, rigidity.
Treatment involves surgery, multiple blood
products.

Cancer of the Liver


One of the most common tumors in the world
Most common complaintabdominal discomfort
Treatment includes:
Chemotherapy
Hepatic artery embolization
Hepatic arterial infusion (HAI)
Surgery

Liver Transplantation
Used in the treatment of end-stage liver disease,
primary malignant neoplasm of the liver
Donor livers obtained primarily from trauma
victims who have not had liver damage
Donor liver transported to the surgery center in a
cooled saline solution that preserves the organ for
up to 8 hours

Complications

Acute, chronic graft rejection


Infection
Hemorrhage
Hepatic artery thrombosis
Fluid and electrolyte imbalances
Pulmonary atelectasis
Acute renal failure
Psychological maladjustment

NCLEX TIME

Question 1
These laboratory results are expected with
which type
of jaundice?
Indirect serum bilirubin: Increased
Direct serum bilirubin: Normal
Stool urobilinogen: Increased
Urine urobilinogen: Increased
A.
B.
C.
D.

Intrahepatic
Hemolytic
Obstructive
Hepatocellular

Question 2
A possible outcome for the patient receiving a liver
transplant because of hepatitis Cinduced cirrhosis
is that the newly transplanted liver may
A. Be a likely site for cancer growth in the future
B. Make the patient more likely to develop
obstructive jaundice in the future
C. Become re-infected with the hepatitis C virus
D. Make the patient more susceptible to develop
other forms of hepatitis

Question 3
Which assessment parameter requires
immediate
intervention in a patient with severe ascites?

A.
B.
C.
D.

Shallow respirations, rate 36 breaths/min


Low-grade fever
Confusion
Tachycardia, rate 110 beats/min

Question 4
A priority intervention in the management of a patient
with decompensated cirrhosis would be:
A.
B.
C.
D.

Limit protein intake.


Monitor fluid intake and output.
Manage nausea and vomiting
Elevate head of bed >30 degrees

Question 5
Which racial group is at the highest risk for
developing
liver cancer?
A.
B.
C.
D.

Caucasian
African American
Asian
Hispanic/Latino

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