Hepatic and Biliary dysfunction
•Diagnostic and clinical manifestations
•Hepatic disorders
•Pancreatic disorders
•The nursing processes
Functions of the liver
• It receives nutrients-rich blood from GIT
• It stores, transforms these nutrients into chemicals to be used by the
body
• Regulates glucose and protein metabolism
• Manufactures and secretes bile for the digestion of fat
• Removes waste products and secretes them into bile
• The bile produced is stored in the gallbladder
• Ammonia conversion: as a result of gluconeogenesis
• Vitamins & iron storage
• Bile formation
• Drug metabolism
Anatomy & location
• Behinds the ribs, in the upper portion of the abdominal cavity
• Weighs 1200-1800 g
• Divided into 4 lobes, separated by a thin layer of connective tissues;
dividing the liver into small functional units, lobules
• 80% of blood supply comes from portal vein; the remainder from hepatic
artery –rich in Oxygen
• hepatic capillaries—sinusoids of liver—venules—composing the central
vein—join to form the hepatic vein
• Phagocytic cells, Kuffer cells are present in the liver
Anatomy & location
• Canaliculi receives bile from hepatocytes—to a larger bile duct—to form
the hepatic duct.
• Hepatic duct joins the cystic duct from gallbladder to form the common
bile duct—that empties into small intestine
• Sphincter of Oddi, in the duodenum, control the flow of bile
Bile formation
• Secreted by hepatocytes
• Composed of water & electrolytes, lecthin, fatty acids, cholesterol,
bilirubin.
• Bile is synthesized from cholesterol after conjugation with amino acids
(taurine& glycine)----required for emulsification of fats
• Bilirubin is derived from moglobin then, conjugated which become more
soluble ,
• The conjugated bilirubin is secreted by hepatocytes and carried out in
bile into duodenum.
• In small intestine, it is converted into urobilinogen –excreted by feces or
some is reabsorbed into portal circulation , some enter the systemic
circulation and by kidneys.
• Bilirubin increased in blood; in liver disease, gall bladder disese,
destruction of RBCs
Hepatic dysfunction
Diagnostic evaluation
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Liver function test
70% of parenchyma may be damaged before abnormal findings appear
Function is measured as serum enzymes:
Aminotransferase; alkaline phosphate; lactic dehydrogenase---released
by liver cells damage --liver injury
• Serum proteins: albumin & globulins, ammonia---liver impairment
• Clotting factors and lipids; prothrombin time---liver cells damage
• Bilirubin: liver and biliary tract disease, Jaundice
Diagnostic evaluation
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Liver biopsy: Table 39-1, P 1290.
Obtain a sample of liver tissue via needle aspiration
Indications: diffuse disorders of the parenchyma
Major complications: bleeding, bile peritonitis---obtain coagulation studies
before biopsy
Liver biopsy can be performed:
Percutaneously under ultrasound guidance
If ascites or coagulation abnormalities; other techniques are preferred
Transvenously through right internal jugular vein-to-right-hepatic vein under
fluroscopic control
 Other diagnostic tests: CT; MRI
 Laboroscopy: insertion of fiberobtic endoscope via small abdominal incision
to examine liver and pelvic structure; To obtain biopsy
Manifestation of hepatic dysfunction
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Hepatic dysfunction results from primary liver disease, or
Indirectly: obstruction of bile flow; derangement of hepatic circulation
Can be acute or chronic; chronic is more common—chronic:
Liver cirrhosis—40% of deaths associate alcohol use
Uncommon, compensated and subclinical Cirrhoses ; often goes
undetected
• Causes of hepatocellular dysfunction: infectious agents, anoxia,
metabolic disorder, nutritional deficiencies-alcohol related
• Parenchymal damage: Noxious agents—liver cells replace glycogen with
lipids—producing fatty infiltration—cell death or necrosis
• Manifestations: jaundice, portal hyertension, ascites and varices,
nutritional deficiencies and hepatic encephalopathy.
Most common clinical manifestations
Jaundice
 Jaundice: abnormal elevation of bilirubin (exceeds 2.5 mg/dL)
 Body tissues, including skin & sclerae, become tinged or greenish-yellow
 Increased serum bilirubin may result from impairment of hepatic uptake,
conjugation, excretion of bilirubin into biliary system
 There are different types of jaundice:
 Hemolytic Jaundice:
 An increased destruction of the red blood cells—the liver can not excrete
 Occurs in hemolytic disorders; transfusion reaction
 The bilirubin ,in blood, is unconjugated or free
 Fecal & urine urobilinogen are increased; urine is free from bilirubin
 May have no symptoms, however, if exceeds 20-25 mg/dL---predispose
brainstem damage; prolonged mild jaundice-- gallbladder stone; severe
jaundice
Most common clinical manifestations
Jaundice
 Obstructive Jaundice:
• Results from extra-hepatic obstruction due to gallbladder enlargement
• Intra-hepatic obstruction: pressure on bile ducts within the liver; by
inflammatory swelling of the liver or from
• Stasis and inspissation (thickening) of bile within canaliculi-obstruction—
after ingestion of medications: Phenothiazines, antithyroid, Sulfonylurea,
tricyclic antidepressant…
• In obstruction—bile can not flow into intestines—backed up in the liver--reabsorbed into blood—staining skin, mucous membrane, sclerae; stool
become clay colored;excreted in the urine—becomes orange and foamy
• Skin—severely itching requires soothing bath
• Dyspepsia and intolerance to fatty foods
• Serum bilirubin and alkaline phosphate are elevated
Most common clinical manifestations
 Hepatocellular Jaundice
• Damaged liver cells are unable to clear bilirubin from blood
• Causes of damage: hepatitis viruses, medications, chemical toxins,
alcohol
• Cirrhosis of liver is a form of hepatocellular disease that produces
jaundice; associate excessive alcohol use
• Patients may experience mild or severe illness
• Associated manifestations: loss of appetite, nausea, fatigue, possible
weight loss
• Serum bilirubin and urine urobilinogen may be elevated
• If the cause is infection, patients may report headache and fever
• May be completely reversible depending on the cause and extent of
damage
Most common clinical manifestations
 Hereditary hyperbilirubinemia
• Results from several inherited disorders, Gilbert’s syndrome---increased
un-conjugated serum bilirubin
• Liver histology and function are normal
• No hemolysis
Most common clinical manifestations
Portal Hypertension
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Increased pressure in the portal venous system
Associates damaged liver that causes obstruction of blood flow
It associates hepatic cirrhosis; although occurs with non-cirrhotic liver
Manifestations: splenomegaly
Consequences: ascites and varices
Ascites
 Contributing factors:
 Damaged liver—portal hypertension—increased capillary pressure &
obstruction of venous blood flow
 Vasodilation in the splanchnic circulation
 Failure of the liver to metabolize Aldosterone—Na & water retention
with:
 Increased intravascular fluid volume
 Increased lymphatic flow
 Decreased synthesis of albumin
 All contribute to movement of intravascular fluid into peritoneal space
 Fluid in the peritoneal space—further retention; Na & water retension
 Albumin-rich fluid moves into peritoneal space; 15 L
Ascites
assessment and clinical manifestations
• Flank bulges with supine position
• Percussion dullness and fluid shifting
• Measure abdominal girth and weight daily to assess progress
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Manifestations:
Increased abdominal girth
Shortness of breath; patients feel uncomfortable
Striae & distended vein may be visible
Fluid & electrolytes imbalances
Ascites
nursing and medical management
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Dietary modifications: negative sodium balance to reduce retention
Avoid salty foods; low-sodium diets (2g sodium) is recommended
Substitute salts with lemon juice
Avoid substitutes that cause Ammonia;
Avoid substitutes that contain K if the patient has renal impairment
May reduce Na intake to 500 mg
If no responses with Na restriction; diuretics
Ascites
nursing and medical management
 Diuretics:
• Sodium restriction + diuretics are successful in 90%
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First line: Spironolactone (Aldactone)
Is an aldosterone blocking agent
For ascites from cirrhosis
Preserves K
• Furosemide (Lasix); may be added
 Long-term use may induce hyopnatremia
Ascites
nursing and medical management
 Diuretics:
• Ammonium chloride & Acetazolamide (Diamox) may precipitate hepatic
coma—contraindicated
• Daily weight loss should not exceed 1-2Kg in patient with ascites and
edema; 0.5-0.75 in patients without edema
• No fluid restriction unless serum Na is very low
• Complications of diuretics:
 Fluid & electrolytes disturbances;
 Encephalopathy from dehydration and hypovolemia;
 Impaired cerebral functioning when K is very low and serum ammonia
increased
Ascites
nursing and medical management
• Bed rest:
• Upright posture—activation of renin-angiotensin-aldosterone system &
sympathetic nervous system—reduced glomerular filtration & Na
excretion—decreased response to loop diuretics
• Bed rest is useful for those refractory to diuretics
Ascites
nursing and medical management
 Paracentesis: removal of fluid from peritoneal cavity via a
puncture/small incision in the abdominal wall
• Ultrasound guidance may be indicated in patients with abnormalities:
coagulation, adhesions
• Is currently performed for diagnostic purposes; in massive ascites—
refractory to nutritional and diuretic therapy
• Ascitic fluid for: cell count, albumin and proteins, culture
• Removal of 5-6 liters is a safe procedure + IV infusion of salt-poor
Albumin/other colloids is a standard management approach
• Albumin infusion helps to correct decrease in effective arterial blood
volume
• Read guidelines for assisting patients with paracentesis (P 1126, Chart
39-3). Transjugular intrahepatic portosystemic shunt.
Nursing management
home & community based care
• For hospitalized: Assessment of fluid status; intake & output; abdominal
girth; daily Wt.
 Assessment of electrolytes balance: serum ammonia, electrolytes,
indications of encephalopathy
• Teaching self-care:
• Avoid alcohol intake
• Adhere to low sodium diet, medications
• Skin care and the need for daily Wt.
• To report sign & symptoms of complications
• Assess home environment & resources available
• Assessment of adherence to treatment plan
• Keep up with appointments
Esophageal Varices
• Occur In majority of patients with cirrhosis
• Are varicosities develop from elevated pressure in veins that drain into
portal system
• Are prone to rupture—source of massive hemorrhage from upper GI
tract and the rectum
• Coagulation abnormalities increase bleeding & blood loss
• Are the significant source of bleeding, In liver cirrhosis
• Varices once form, they increase in size and bleed
• First bleeding has a mortality rate of 30-50%
Esophageal varices
pathophysiology
• Are dilated tortuous veins in submucosa of lower esophagus
• Damaged liver—obstruction of portal venous circulation—portal
hypertension
• Because of obstruction—venous blood from intestinal & spleen tract
seeks outlet through collateral circulation to right atrium—tortuous &
fragile—rupture & bleed
• Are life-threatening—hemorrhagic shock—leading to--decreased
hepatic, cerebral, renal perfusion
• Bleeding in GI—increased nitrogen load & serum ammonia—increased
risk of encephalopathy
• Contributing factors to hemorrhage: muscular exertion-heavy lifting;
straining, sneezing-vomiting-coughing; irritating foods, reflux of stomach
content (Alcohol); Salicylates
Esophageal varices
Diagnoses and assessment
• Signs of bleeding: hematemesis, melena, deterioration in mental &
physical states; history of alcohol abuse
• Signs of shock: cool clammy skin, hypotension, tachycardia
• Endoscopy, barium swallow, CT, angiography
• In patients with cirrhosis—screening endoscopy every 2 years to identify
& treat large varices
• Careful monitoring can detect early signs of cardiac dysrhythmias,
perforations, hemorrhage
 After examinations:
• Fluid are not permitted until gag reflex returns
• Lozenges & gargles to relive throat discomfort if physiologically
permitted
• No oral intake in active bleeding
Portal hypertension measurement
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Indications: dilated abdominal veins, hemorrhoids, splenomegaly,ascites
Indirect measurement of hepatic vein pressure is the most common
Insertion of a catheter with a balloon into antecubital or femoral vein
Then advanced under fluoroscopy to a hepatic vein
Fluid is infused to inflate the balloon
A wedged pressure is obtained by occluding blood flow
Pressure in the un-occluded vessel is obtained
Direct measurement: Laparotomy—needle in spleen—manometer
More than 20 ml saline is abnormal
Blood tests: liver function tests—serum aminotransferase, bilirubin,
alkaline phosphate, serum proteins
Esophageal varices
Nursing and medical management
• Bleeding from EV requires aggressive medical care, expert nursing, ICU
for frequent vital signs measurement
• Monitoring for indicators of hemorrhagic shock
• Central venous pressure to evalute blood volume and arterial line
• Oxygen to prevent hypoxia & maintain adequate blood oxygenation
• IV fluids, electrolytes & expanders to restore blood volume
• Transfusion of blood components may be required
• Caution: overhydration—raise portal hypertension—increases bleeding
• Indwelling urinary catheter to monitor urine output
• Nonsurgical management minimizes risk of mortality; and because of
poor physical condition related to severe liver dysfunction
Esophageal varices
pharmacologic therapy
• In active bleeding; Vasopressin (Pitressin) produces constriction of
splanchnic arterial bed—reducing blood flow in the portal system &
decreases portal hypertension
• Effectiveness of vasopressin: vital signs and blood-free gastric aspirate
• Has anti-diuretic effect and hyponatremia may develop: monitor intake
& output, electrolytes
• Contraindicated in CADs; can be used with nitroglycerin
• Side effects of vasopressin: ischemia & dysrhythmias; add nitroglycerin
• Somatostatin & Octreotide (Sandostatin) effective in decreasing
bleeding; has no vasconstrictive effect; have selective effects
• Other medications: propranolol & nadolol, Beta blocker agents—
decrease portal pressure—prevent bleeding episodes; Beta-blockers
should not be used in acute hemorrage; just as prophylaxis
• Nitrates (isordil): lower portal pressure by venodilation.
Esophageal varices
balloon tamponade
• To control hemorrhage; exertion of pressure on the cardia by a doubleballoon tamponade
• Sengstaken-Blakemore tube has 4 openings: gastric aspiration,
esophageal aspiration, balloon inflation (gastric & esophagus)
• In stomach, Inflated with 100-200 ml of air; then pulled & traction
applied; pressure in esophageal & gastric balloons is 25 – 40mm HG
• Continuous low suctioning with hourly irrigation to detect bleeding
• Irrigastion; and Pressure measurement every 2-4 hours to prevent
esophageal injury & under-inflation
• After several hours of no bleeding, can be deflated safely; if still no
bleeding can be removed
• Danger: displacement, inflation into oropharynx, rupture—pulmonary
aspiration—ET tube to protect from aspiration ; necrosis—long period
Esophageal varices
other medical management
 Endoscopic sclerotherapy:
• Injection of sclerosing agent into esophageal varices via fiberobtic
endoscope—to promote thrombosis
• After treatment observe for bleeding, perforation of esophagus,
esophageal stricture, aspiration pneumonia
• Antacids, Cimetidine or Pantoprazole (Protonix), a proton pump inhibitor
may be given to counteract the sclerosing agent
 Surgical management:
 Variceal banding
 Portal systemic shunt
 Read management modalities (Table 39-2 P. 1134)
Esophageal varices
nursing actions
• Continuous monitoring of physical, emotional & mental status
• Assess vital signs & nutritional status
• GI bleeding-elevated serum ammonia causing drowsiness to profound
coma
• Parenteral nutrition if complete rest of esophagus is indicated
• Gastric suctioning to prevent straining & vomiting
• Frequent oral hygiene & moist sponge to the lips to prevent thirst feeling
• blood transfusions & Vit K therapy
• Quiet environment & reassurance to relieve anxiety
• Delirium secondary to alcohol withdrawal may occur; anxiety
• Provide support & explanation about medical therapies
Hepatic encephalopathy and coma
• Porto-systemic encephalopathy is a life-threatening complication occurs
with liver failure
• Is neuropsychiatric manifestation of hepatic failure associates portal
hypertension or shunting of blood from portal into systemic circulation
• Is a reversible metabolic form of encephalopathy
• Can improve with recovery of liver function
• Occurs in stages; (read Table 39-3, P 1132)
Hepatic encephalopathy
Pathophysiology
• Occurs because
 Inability of liver to detoxify toxic byproducts of metabolism
 Shunting allows elements of portal blood to enter systemic circulation;
collateral circulation
• Ammonia is the major etiologic factor—enter the brain—increasing
neuro-steroid synthesis; that stimulates gamma aminobutyric acid—
causing depression of the CNS
• Ammonia inhibits neurotransmission & synaptic regulations—producing
sleep & behavior patterns that associate hepatic encephalopathy
Hepatic encephalopathy
Pathophysiology
• Major source of ammonia: enzymatic & bacterial digestion of dietary &
blood proteins in GI
• Other factors that increases ammonia are GI Bleeding; high protein diet;
bacterial infection; uremia
• With alkalosis / hypokalemia increased amount of ammonia is absorbed
from GI.
• Serum ammonia is decreased by:
 Elimination of protein from the diet
 Administration of antibiotics, Neomycin sulfate; decreases intestinal
bacteria that covert urea to ammonia
Hepatic encephalopathy
assessment and diagnosis
• EEG: generalized slowing, increased amplitude of brain wave
• Early symptoms: minor mental changes and motor disturbances;
• Confusion with altered mood & sleep pattern—tends to sleep during day
with restlessness & insomnia at night
• With progress, disorientation to time & place
• Further progression: frank coma, Seizures
• Other manifestations:
• Asterixis: flapping tremor of hands; also hand writing becomes difficult,
seen in stage 2,
• Constructional apraxia: inability to reproduce a simple figure
• Fetor hepaticus: fecal odor to the breath; is prevalent in extensive
collateral circulation
Hepatic encephalopathy
medical management
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Principle of management
Elimination of precipitating factors
Initiating ammonia-lowering therapy
Minimizing potential complications of cirrhosis & coma
Reversing the underlying liver disease
Lactulose: orally; or by nasogastric tube or enema if orally is not allowed
Reduces serum ammonia by promoting excretion of ammonia in stool
Monitor for watery diarrheal stool
Side effects: intestinal bloating & cramping
Can be diluted with fruit juice to mask sweet taste
Monitor for hypokalemia, dehydration
Other laxatives are not prescribed with lactulose intake
Hepatic encephalopathy
medical management
• IV glucose to minimize protein breakdown
• Vitamins to correct deficiencies, correction of electrolytes, K
• Antibiotics: neomycin, Flagyl, Rifaximin to reduce ammonia forming
bacteria
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Additional principles of management
Assess mental status, daily handwriting
Daily intake & output, weight
Protein intake is moderately restricted—for comatose patients
Vital signs every 4 hours, serum ammonia daily
Assess potential sites of infection, peritoneum, lungs
Read page 1136 for further principles of management of encepahlopathy
Hepatic encephalopathy
medical management
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Moderate restriction of protein intake
Long-term restriction-less than 1 gm / Kg daily should be avoided
Vegetables or dairy proteins can be used; UP TO 12O Gms/day
Advised: Food high in proteins, meat, eggs, should be eliminated from
the diet for short-term. (Read chart 39-5, P 1136).
Enteral feeding if encephalopathy persists
Monitor and correct electrolyte status; I & O
Discontinue Sedatives, Tranquilizers, analgesics
Flumazenil (Romazicon), a Benzodiazepine antagonist may be given to
improve encephalopathy
Reduction of ammonia absorption by gastric suction, enema, antacids
Hepatic encephalopathy
nursing management
• Maintain safe environment to prevent injury, bleeding, infection
• Prevent respiratory complications
• Family support and reassurance
 Teaching self care:
 Watch for subtle signs of recurrent encephalopathy
 Restriction of protein intake (0.8-1 gm/Kg daily), moderate protein-High
caloric diet
 Use of vegetable proteins
 Use of lactulose to prevent constipation
Viral hepatitis
• Is a systemic viral infection-necrosis & inflammation of liver cells
produce a cluster of clinical, biochemical & cellular changes
• Definitive types of hepatitis are A, B ,C,D,E
• Is easily transmitted
• Causes morbidity & prolonged loss of time from school or employment
• Occurrence rate has been decreased because of A & B vaccines & public
education
Hepatitis A Virus
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HAV accounts for 20-25% of cases of clinical hepatitis
Caused by RNA virus; HAV
Is seen mainly in adult population
Transmitted through fecal-oral route-ingestion of food-liquid infected
More prevalent in overcrowding & poor sanitation places; as a result of
poor hygiene
Virus is found in the stool of infected persons before symptoms onset &
during the first few days of illness
Can be transmitted during sexual activity
Incubation period 2-6 weeks; M = 4 Weeks
Rarely progresses to acute liver necrosis / cirrhosis
No carrier state exists; the virus presents briefly in the serum
HAV
Assessment & diagnosis
• Many Patients are anicteric (no Jaundice) & symptomless
• If symptoms present: Resemble mild flulike of upper respiratory tract
infection with Low-grade fever
• Severe anorexia—an early symptom—result from release of toxins from
the damaged liver or inability of the liver to detoxify abnormal products;
Later; jaundice & dark urine
• indigestion with epigastric distress, nausea, heartburn, flatulence
• A strong aversion to taste of cigarettes
• Symptoms tend to clear as jaundice reach the peak, 10-days after
appearance
• Liver & spleen enlargement; hepatitis A antigen in the stool
• HAV antibodies in the serum
HAV
Prevention
• Scrupulous hand washing, safe water supplies, proper control of sewage
disposal
• Vaccination: 2 times for adult, 18-year or older with 6-12 months apart
 3 times for children with 1-month & 6-12 months apart
 For those with no vaccination; IM of globulin during incubation period
 Medical management:
• Bed rest; acceptable & nutritious diet
• In anorexia: Frequent small feedings supplemented by IV fluids with
glucose
• Optimal food & fluid intake to prevent weight loss & to speed recovery
• Gradual progressive ambulation may hasten recovery
• Teach patient to: Avoid alcohol; Have proper hygiene; Seek care
• Read charts: 39-7 and 39-8; P. 1141
Hepatitis B virus
• Transmitted through blood; percutaneous or permucosal routes
• Or from carrier mother to their infants at time of birth
• Found in blood, saliva, semen, vaginal secretions; has a long incubation
period; replicates in the liver & remains in serum
• Who contract HBV develop antibodies and recover within 6 months
• 10% progress to carrier or develop chronic hepatitis—hepatocellular
injury & inflammation
• In elderly may progress to severe cell necrosis or hepatic failure; because
of alteration in the immune system
• So, factors that affect liver function should be eliminated; medications,
alcohol
• Risk Factors; read chart 39-9, P. 1141.
HBV
assessment & diagnosis
• Symptoms similar to that of HAV; although are rare; much longer
incubation period, 1-6 months
• Arthralgia, rashes
• Loss of appetite, dyspepsia, generalized aching , malaise & weakness
• Jaundice with dark urine& light-colored stool may appear
• Liver tender and enlarged; spleen is enlarged
• Has different antigen: HBcAg; HBsAg, HBeAg, HBxAg
• For each antibodies are developed: anti HBs, HBc, Hbe, HBx.
• HBsAg appear in 90% ; if persists for more than 6 months; patient is a
carrier
HBV
Prevention
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General precaution to prevent transmission
Screening blood donors; Read preventing transmission, P. 1142.
Precautions related to healthcare providers
Immunization
Active immunization with Recombivax HB
for those at high risk: healthcare providers, hemodialysis patients, &
those with hepatitis C
 Has an effect for 5-10 years, booster doses for immunocompromised
patients
 Given IM in 3 doses; with 1 & 6 months apart, in the deltoid muscle
• Passive immunity: HBIG, hepatis B immune globulin; for those exposed
to HBV given within hours to few days
HBV
Medical management
• Alpha-interferon: 5 million units daily or 10 million units 3 times a week
for 16-24 weeks
• Side effects: fever, chills, anorexia, nausea, fatigue
• Delayed side effects: bone marrow depression, thyroid dysfunction,
alopecia,; may necessitate reduction of the dose
• Antiviral agents may be used: Lamivudine, Adefovir
• Bed rest may be recommended until symptoms subsided;
• Activity is restricted until liver enlargement & serum bilirubin are
decreased
• Maintain adequate nutrition; protein restriction may be required; if liver
ability to metabolize proteins is impaired
• In case of vomiting, hospitalization for fluid replacement
HBV
Nursing actions
• Convalescence period: 3-4 months
• Identify psychosocial responses
• Teach and provide necessary steps in medical management
• Read Table 39-4, P 1139 for other forms of Hepatitis
Hepatic cirrhosis
 Is a chronic disease in which liver tissues are replaced by diffuse fibrosis
that disrupts structure & function of the liver
 Types of cirrhosis:
• Alcoholic cirrhosis: scar tissue surrounds portal area
• Postnecrotic cirrhosis: there are broad bands of scar tissue, a result of
acute viral hepatitis
• Biliary cirrhosis: scarring around bile ducts, a result of chronic biliary
obstruction
Hepatic cirrhosis
pathophysiology
• Major causative factors: Alcohol consumption; nutritional deficiency;
exposure to certain chemicals, carbon, arsenic, phosphorus
• Alcoholic cirrhosis: episodes of liver cells necrosis—replaced by scar
tissues—exceeds that of functioning liver tissue—re-generating liver
tissue project from constricted areas giving hobnail appearance
• Severity of symptoms characterizes cirrhosis as
• Compensated: has vague symptoms, discovered accidently
• Decompensated: results from failure of the liver to synthesize proteins,
clotting factors, other substances; complications
• Manifestations: Hepatic dysfunction manifestations; edema, GIT:
distended abdominal BVs; vitamins deficiency & anemia; mental
deterioration. READ TABLE 39-5 & CHART 39-11; P. 1147.
Hepatic cirrhosis
medical management
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Depends on Symptoms
Antacids & antihistanie-2 to minimize GI bleeding
Vitamins and nutritional supplements promote healing
Diuretics for ascites; spironolactone to decrease ascites
• Colchicine has anti-inflammatory effect may increase survival time
• Some medications show antifibrotic effect, statins, diuretics,
immunosuppressants
• In ESLD, Herb milk thistle: has anti-inflammatory effect & antioxidant
properties
• Ursodeoxycholic acid for biliary cirrhosis to improve liver function
Hepatic cirrhosis
nursing actions
• Read chart 39-12, P 1150-1157 for more details
 Promoting rest:
• To decrease demands on the liver & increases liver’s blood supply
• Adjust position for respiratory efficiency, O2 therapy to prevent cell
destruction;
• Measures to prevent complications of immobility
• Weight, and intake & output daily
• Encourage gradual increase in activity once nutritional status improves
Hepatic cirrhosis
nursing actions
 Improving nutritional status:
• In cirrhosis without edema, ascites or sign of hepatic coma; give a
nutritious high protein diet supplemented by vitamins
• In ascites, frequent small meals; consider patients preferences
• In severe anorexia, enteral or parenteral feeding may be given
• In patient with fatty stool (steatorrhea), give water-soluble vitamins: A,
D&E
• In impending coma decrease protein in the diet; if encephalopathy
develops, restrict protein intake
• Vegetable protein to meet the patient needs
• Sodium restriction in ascites
Hepatic cirrhosis
nursing actions
 Providing skin care: because of subcutaneous edema, immobility,
jaundice,
• Frequent position changes
• Avoid irritating soap & adhesive tape to prevent trauma
• Lotion to sooth irritated skin, minimize scratching
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Reducing risk of injury:
Prevent fall, padded side rails
Minimize agitation by orientation to time & place, explain all procedures
Minimize bleeding; electronic razor, soft-bristled toothbrush, pressure to
all venipuncture