Download LeMone p. 580-585

NOTES
Module 14: Gastrointestinal: Liver- Hepatitis/Cirrhosis of the liver
Marnie Quick, RN, MSN, CNRN
Etiology/Pathophysiolgy
1.
Normal liver pathology as it relates to hepatitis/cirrhosis of the liver
a. Carbohydrate metabolism1) Stored as glycogen.
2) Glucose level depends on livers’ ability to remove glucose
from blood, store it, break it down, and release it again.
b. Protein metabolism1) Protein breakdown begins in the GI track where ammonia is
formed by the breakdown of protein (from food or blood in
the GI track) by the bacteria in the GI track. The ammonia
is normally converted by the liver to form urea.
2) Liver synthesizes plasma proteins- prothrombin, fibrinogen,
and albumin (these alter blood clotting and serum osmotic
pressure) Increased calorie intake helps increase this
synthesis.
c. Fat metabolism1) Fat is converted to triglycerides, cholesterol, phospholipids,
and lipoprotein; then to glycerol and fatty acids called
ketogenesis.
2) When the liver is damaged get decreased synthesis and
transport of cholesterol.
3) Biliary obstruction results in decreased excretion, excess
cholesterol is deposited in the liver.
d. Steroid metabolism1) Estrogens are unmetabolized and deactivated by the liver
and excreted in bile.
2) Aldosterone metabolism- if liver not working get increased
levels and this causes Na and H2O retention.
3) Steroids should be used with caution in patient with liver
disease.
e. Bile formation and secretion (500-1000cc/day)1) Bile aids in digestion and absorption of fats in small
intestine.
2) Unconjugated or indirect bilirubin is broken down to
urobilinogen which is excreted in stool and gives it color
f. Storage of vitamins1) A, and B’s, D, E, and K
g. Regulates blood coagulation1) Liver forms blood constituents and maintains flow of blood.
Prothrombin, fibrinogen, and heparin.
2) In liver disease have decrease of Vit K and fibrinogen which
causes increased fibrinolysis and decreased platelets which
leads to hemorrhage
h. Detoxification1) in liver failure, endogenous products accumulate in blood,
lead to hepatic coma
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2.
3.
4.
i. Heat production- 2nd only to muscle tissue.
Individual will begin to show symptoms when 80% liver destroyed
The liver can regenerate itself if adequate nutrition and no alcohol.
Has dual blood supply
a. Hepatic artery carries oxygenated blood to liver (400 cc)
b. Portal vein carries partly oxygenated blood to the liver (1000 cc) and
supplies 50-60% of O2 needs of the liver.
Hepatitis
Etiology/Pathophysiology of Hepatitis
1. Hepatitis is inflammation of the liver
a. Viral- most common cause of inflammation of the liver.
1) Chronic- Hepatitis B, C, and D cause a chronic form. Chronic
is the primary cause of liver damage leading to cirrhosis and
liver cancer
2) Fuminant- rapidly progressive form related to HBV with HDV.
Liver failure in 2-3 weeks.
b. Toxic- Hepatoxins directly damage liver which result in necrosis.
Hepatoxins include chronic alcohol abuse; drugs such as
acetaminophen; chemicals such as benzene, carbon tetrachloride
c. Hepatobillary- Disruption of the flow of bile out of the liver.
2.
Viral hepatitis (p 581 Table 22-2)
a. Hepatitis A virus (Infectious hepatitis)
1) Fecal-oral transmission.
2) Contaminated food, unsanitary conditions, water, shelfish and
direct contact with infected person. Individual is contagious
through stool up to 2 wks before symptoms appear- flu like
symptoms 1-2 weeks before jaundice appears
3) Incubation period 2-6 weeks.
4) Onset abrupt, benign and self-limiting, symptoms last up to 2
months; liver usually repairs itself so no permanent effects.
No chronic state of Hepatitis A.
5) Vaccine- 2 doses IM
6) Postexposure prophylaxis- standard IG-immune globulin, IM
within 2 weeks of exposure.
7) 2/2/2/2 rule- 2 doses IM to prevent; S&S last 2 months;
contagious 2 wks before S&S; post exposure dose given IM
within 2 wks of exposure.
b. Hepatitis B
1) Blood and body fluid transmission
2) High risk health care workers exposure to blood and needle
sticks, IV drug users, multiple sex partners, men who have
sex with other men, body piercing, tattoos, and individuals
exposed to blood products as hemodialysis. Frequently seen
with HIV. More infectious than HIV.
3) Incubation period 6-24 months
4) Liver damage is by immune response to ‘B’ antigen.
5) Increased risk for primary liver cancer; causes acute and
chronic hepatitis or fulminant hepatitis.
6) May become chronic carrier. Vaccine- 3 doses IM, 4-6
weeks apart.
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7)
Post exposure- hepatitis B immune globulin, IM in 2 dosesdose 1st within 24 hrs-7 days post exposure; dose #2 28-30
days post exposure. Interferon alpha (antiviral) in Chronic
‘B’.
c. Hepatitis C (formerly known as non A, non B)
1) Blood and body fluid transmission
2) Injection (IV) drug users (primary cause), blood
transfusions, body piercing, tattoos.
3) Initial symptoms mild, nonspecific
4) Primary worldwide cause of chronic hepatitis, cirrhosis, and
liver cancer. May be 10-20 year delay between infection and
clinical appearance of liver damage.
5) Interferon alpha to reduce risk of chronic ‘C’ given with
Ribavirin (oral antiviral)
d. Hepatitis D
1) Blood and body fluid transmission.
2) Causes infection in people who also have hepatitis B.
3) Causes acute and chronic infections.
e. Hepatitis E
1) Transmission- oral-fecal.
2) Contaminated water supply in developing countries.
3) Rare in the US.
Common Manifestations/Complications of Hepatitis (p.581 box)
1.
Incubation Phase- after exposure to virus, no symptoms
2.
Preicteric Phase of hepatitis - ‘Flu-like’ symptoms-general malaise, fatigue,
muscle and body aches; GI symptoms- nausea/vomiting,
diarrhea/constipation; mild right upper abdominal pain; chills and fever.
3.
Icteric or Jaundice Phase- jaundice of the sclera, skin and mucous
membranes; pruitus; clay colored stools; brown urine (all caused by
elevation of bilirubin). Usually 5-10 days after preicteric symptoms
4.
Posticteric/Convalescent Phase- Serum billirubin and enzymes return to
normal; energy level increases; no pain; GI symptoms minimal.
5.
Healing generally within 3-16 weeks. Uncomplicated cases recovery occurs
within 2 weeks of jaundice.
6.
Complications of some forms of hepatitis- cirrhosis, liver failure.
Therapeutic Interventions for Hepatitis
1.
Diagnostic tests
a. ALT (specific to liver), AST (liver and heart)- enzymes released into
blood when liver cells are damaged.
b. Bilirubin- elevated in viral hepatitis because of impaired bilirubin
metabolism, obstruction of hepatobiliary ducts due to inflammation
and edema
c. Viral antigens & their specific antibodies (p 581 Table 22-2)
d. Liver biopsy-detect chronic hepatitis(p.590 Fig 22-3/Nsg impl box)
1)
Pre biopsy: Check lab- PT, platelet count, coagulation
studies, may need Vit K to correct
2)
Explain procedure.
3)
NPO 4-6 hrs and empty bladder prior.
4)
Place in supine position on far right side of bed; turn head
to left and extend arm above head.
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5)
2.
3.
Post biopsy- pressure applied to site, place on right side to
maintain site pressure
VS every 2 hrs
Food and fluid withheld for 2 hrs post
Avoid coughing, lifting, or straining for 2 weeks
6)
7)
8)
Medications
a. Vaccines (available for Hepatitis A and B) Hepatitis B is
recommended for high-risk group.
b. Post exposure prophylaxis recommended for household and sexual
contacts of individuals with HAV or HBV.
c. Hepatitis A prophylaxis; single dose of immune globulin within 2
weeks of exposure.
d. Hepatitis B prophylaxis: Hepatitis B immune globulin (HBIG) for
short-term immunity; HBV vaccine may be given at the same time
e. Treatment medications: Interferon alpha (chronic B & C); lamivudine
(chronic B); and ribavirin (given with interferon alpha as the
treatment of choice for chronic C).
Acute hepatitis treatments
a. Bedrest as needed; avoid strenuous activities
b. Adequate nutrition
c. Avoid substances toxic to the liver, especially alcohol.
Nursing Assessment Specific to Hepatitis.
1.
Health history
a. current symptoms, exposure to hepatitis, high risk activities, current
medications
2.
Physical assessment
a. Vital signs esp temperature; color of sclera, skin, stool; abdominal
tenderness; GI complains- nausea, etc; lab tests.
Pertinent Nursing Problems and Interventions for Hepatitis
1.
Risk for infection (transmission)
a. Educate- dependent on type- hygiene; handwashing, especially for
food handlers; blood and body fluids precautions; vaccines for
persons at high risk
b. Report to health department food handler or child care worker with
Hepatitis A
2.
Fatigue- adeq rest; may not be able to resume normal activity 4 wks.
3.
Imbalanced nutrition: less than body requirements
a. High caloric diet with adequate carbohydrates
b. Small frequent meals with nutritional supplements
4.
Disturbed body image- jaundice, itching
5.
Home care
a. Educate
b. Avoid hepatic toxins
c. Need for follow-up
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Cirrhosis of the Liver
Etiology/Pathophysiology of Cirrhosis
1.
Cirrhosis is the end stage of chronic liver disease. It is progressive and
irreversible and results in liver failure.
2.
Functional liver tissue is destroyed and replaced by fibrous scar tissue.
3.
As hepatocytes are destroyed, metabolic functions are lost; blood and bile
flow within liver is disrupted and portal hypertension develops.
4.
Alcoholic/nutritional cirrhosis
a. Most common cause of cirrhosis- alcohol abuse with resultant lack of
nutrition.
b. Stage 1: Metabolic changes affect fatty metabolism, fat accumulates
in liver- fatty liver. In this early stage, abstinence from alcohol could
allow liver to heal.
c. Stage 2: With continued alcohol use, inflammatory cells infiltrate the
liver causing necrosis, fibrosis and destruction of liver tissue.
d. Stage 3: Regenerative nodules form and the liver shrinks.
5.
Biliary cirrhosis
a. Chronic biliary obstruction causing fibrosis of the liver.
b. Jaundice primary symptom
6.
Posthepatic/postnecrotic cirrhosis
a. Post chronic hepatitis B or C, toxic substances cause extensive liver
cell loss and fibrosis.
Common Manifestations/Complications/Treatment for Complications
1.
Early signs may only be enlarged, tender liver. Dull ache in RUQ, weight
loss, weakness, anorexia
2.
Progress to multisystem effects of cirrhosis (p. 587- picture)
3.
Portal hypertension
a. Fibrous connective tissue in the liver disrupt blood and bile flow. This
causes restrictive blood flow from the inferior vena cava and
compression of the portal and hepatic veins- portal hypertension
b. Blood flow is obstructed, increasing pressure in the veins.
c. Veins in the esophagus, rectum and abdomen become
engorged/congested, resulting in esophageal and gastric varices.
d. With this backup of blood, also have acites, splenomegaly, peripheral
edema, anemia and low WBC/platelet (increased blood cell
destruction) see below
e. Treatment: medications to control hypertension; diuretics to
decrease fluid retention and acites.
f. Treatment: surgery- transjugular intrahepatic portosystemic shunt
(TIPS procedure) (p 593 Fig 22-6)
1) Balloon catheter is inserted through the jugular vein to the
hepatic veins.
2) A channel made in the liver and the expandable stent is
inserted into channel.
3) Allows blood to flow from portal vein into hepatic vein,
bypassing the cirrhotic liver.
4) This relieves pressure in the esophageal veins and helps
control fluid retention.
5) Used as short term measure until liver transplant
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4.
5.
6.
Splenomegaly
a. Spleen enlarges as blood shunted into splenic vein
b. Blood cells destroyed- anemia, leukopenia, thrombocytopenia
c. Treatment- treat portal hypertension
Ascites and peripheral edema
a. Ascites- accumulation of plasma-rich fluid in the abdominal cavity.
b. Portal hypertension causes an impairment of liver synthesis of
albumin (hypoalbuminemia) and the accumulation of albumin in
peritoneal cavity. Also with the decrease in renal blood flow have an
increase in aldosterone which results in sodium and water retention.
c. Assess- abdominal distention (girth) and weight gain
d. Treatment- diet: high carbohydrate, protein (depends on stage- not
if experiencing hepatic encephalopathy), low-fat, low-sodium diet
e. Treatment- Medications: diuretics (Aldactone)
f. Treatment- Paracentesis (p. 591 Fig 22-4; p. 592 box Nsg impl)
1)
Considered a temporary treatment for acites
2)
Removal of large amounts of fluid (& protein).
3)
Obtain weight, take VS, and void before
4)
Watch for bleeding after procedure
5)
Salt-poor albumin may be given after to replace lost protein
Esophageal varices (p. 588 picture/manifestations/cause)
a. Dilated tortuous veins in esophagus caused by portal hypertension.
b. Occurs in 60% of individuals with cirrhosis.
c. Major concern- uncontrolled massive bleeding
d. Treatment- Medications
1) Vasopressin to control bleeding.
2) Beta blockers- Nadolo given with isosorbide mononitrite to
prevent bleeding of varices.
3) Blood replacement if bleeding- fresh frozen plasma to
restore clotting factors
4) Vit K correction of clotting abnormalities.
e. Treatment1) Avoid alcohol, aspirin, irritating foods
2) Avoid coughing, anything that increases pressure on varices
f. Treatment1) Shunt- TIPS procedure (see portal hypertension)
2) Surgical ligation of varices
3) Banding- during endoscopy small rubber bands placed on
sclerotic veins to occlude blood flow or a sclerosing agent
injected into veins to cause clotting.
g. Treatment- Sengstaken Blakemore tube- balloon tamponade (p. 592
Fig 22-5) Applies direct pressure on bleeding varices.
1) Physician inserts tube down the mouth into the esophagus.
2) Three lumens- one for gastric aspiration; one inflates
esophageal balloon (25-30 mmHg); and third one inflates
gastric balloon (250 ml air)
3) Tension (traction) is needed to keep to tube in place.
4) Endotracheal tube may be inserted to maintain airway
5) Do not leave in place more than 48 hrs
6) Suction secretions- can not swallow- risk for aspiration.
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7.
8.
Hepatic encephalopathy
a. Caused by accumulated neurotoxins in blood; ammonia produced in
gut is not converted to urea and accumulates in blood; medications
may not be metabolized and add to mental changes.
b. The ammonia is formed in the GI track by the breakdown of protein
(from food or blood in the GI track) by the bacteria in the GI track.
The ammonia is normally converted by the liver to form urea.
Because the liver is nonfunctioning there is a buildup of ammonia in
the blood and ammonia crosses the blood brain barrier and causes
the symptoms of encephalopathy.
c. Medications may not be metabolized, add to mental changes.
d. Stages
1) Onset- personality changes, agitation, impaired judgment,
irritability, slurred speech.
2) Second- hyper reflexia, asterixis (liver flap- flapping tremor
of hands when arms are extended), violent or abusive
behavior
3) Coma- positive Babinski, hyperactive reflexes, unresponsive
e. Treatment
1) Treatment aimed at decreasing ammonia level.
2) Enemas q 6 hrs to decrease ammonia absorption
3) Lactulose is a laxative and it also causes an acid
environment in the GI track. It decreases ammonia level by
decreasing the bacteria in bowel that normally convert
protein to ammonia. It also causes a more acid environment
so that ammonia is converted to ammonium-- which is a
more nonabsorble form. The ammonia and ammonium then
are excreted in the stool (3-4 stools a day). This decreases
the ammonia in the blood, decreasing the symptoms of
hepatic encephalopathy. Given orally or by enema.(p.591)
4) Neomycin- intestinal antiseptic to achieve sterile bowel- this
decreases the bacteria in bowel that normally convert
protein to ammonia. Given orally or enema.
5) Decrease protein intake (60-80 gm/day) - if the liver patient
is experiencing symptoms of encephalopathy then decrease
protein intake. If he is not, then encourage an increase in
protein to help with repair of the damaged liver.
Hepatorenal syndrome
a. Generally felt to be caused by decreased blood to the kidney as a
result of hepatic portal hypertension causing renal failure- decreased
urine output, increased BUM and creatine.
Therapeutic Interventions for Cirrhosis
9.
Diagnostic tests
a. Liver function tests- ALT, AST (elevated, but not as high as acute
hepatitis)
b. CBC with platelets- (anemia, leucopenia, thrombocytopenia)
c. Coagulation studies- (prolonged prothrombin time due to lack of
Vitamin K)
d. Bilirubin- (elevated)
e. Serum albumin (hypoalbuminemia), ammonia (elevated)
f. Abdominal ultrasound (liver size and nodulars, acites)
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10.
11.
12.
g. Esophagascopy for esophageal varices
h. Liver biopsy (p. 590 Fig 22-3- covered in hepatitis section) (not done
if bleeding times are elevated)
Medications (p. 591 box on med administration)
a. Avoid liver toxic drugs- sedatives, hypnotics, acetaminophen,
alcohol.
b. Diuretics to reduce ascites: Spironolactone (Aldactone), furosemide
(Lasix)
c. Lactulose (laxative) and neomycin (antibiotic) to decrease symptoms
of hepatic encephalopathy by reducing number of ammonia forming
bacteria in bowel. (Refer to 7 hepatic encephalopathy: e. Treatment)
and converts ammonia to ammonium which is excreted in stool.
d. Vitamin K to reduce risk of bleeding.
e. Beta-blockers to prevent esophageal varices from rebleeding.
f. Ferrous sulfate and folic acid to treat anemia
g. Antacids to decrease acute gastritis
Dietary and fluid
a. Restricted fluid and sodium intake based on response to diuretic
therapy, urine output, electrolyte values.
b. High calories and protein. (Restrict protein (60-80 g/day if has signs
of hepatic encephalopathy). May need parenteral nutrition (TPN).
c. Vitamin and mineral supplement
Surgery
a. Surgery to treat complications (see above ‘complications’)
b. Liver transplantation (p. 593 Fig 22-6 and box)
Nursing Assessment Specific to Cirrhosis
1.
Health history: current symptoms; altered bowel; excess bleeding;
abdominal distention; jaundice, pruritus, history of liver or gallbladder
disease, alcohol history
2.
Physical exam: VS, mental status, color skin; peripheral pulses and edema;
abdominal assessment, bowel sounds, abdominal girth, tenderness and liver
size.
Pertinent Nursing Problems and Interventions for Cirrhosis
1.
Excess fluid volume
a. Daily weight
b. Low sodium diet
c. Monitor lab- specific gravity, elevated creatinine and BUN, etc
2.
Disturbed thought process
a. Avoid factors that precipitate hepatic encephalopathy
b. Identify symptoms early so treatment started
3.
Ineffective protection
a. Vital signs- assessing for hypovolemia
b. Assess for bleeding- coagulation studies, platelet count, visually
assess for, etc.
4.
Impaired skin integrity
a. Assess jaundice, pruritus, skin breakdown
5.
Imbalanced Nutrition: Less than body requirements
a. Daily weights
b. Small frequent meals in anorexic phase
c. Unless protein restricted (hepatic encephalopathy)- protein
supplements
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6.
d.
Home
a.
b.
c.
d.
e.
f.
g.
Assess sodium/fluid
care
Recommend AA, if cause
Diet and fluid restrictions
Teach medications
Teach about complications- need for follow-up
Teach skin care- pruritus
Teach ways to manage fatigue/conserve energy
Assess need for hospice
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