Liver or Hepatic disorders are common and may result from a virus or exposure to toxic substances such as alcohol. Another liver disorder is cancer: hepatocellular carcinoma is a highly malignant tumor that is difficult to treat and often fatal. Liver function is complex, and liver dysfunction affects all body systems. For this reason, the nurse must understand how the liver functions and must have expert assessment and clinical management skills to care for patients undergoing complex diagnostic and treatment procedures. The liver plays additional roles in detoxification of chemicals and synthesis and storage of important nutrients and The liver is especially important in the regulation of glucose and protein metabolism .

2. 1. Jaundice
2. Hepatic cirrhosis
3. Portal hypertension
4. Ascites
5. Hepatic encephalopathy and coma
6. Liver cancer
7. Liver abscess

3. Liver or Hepatic disorders are common and may
result from a virus or exposure to toxic substances
such as alcohol.
Another liver disorder is cancer: hepatocellular
carcinoma is a highly malignant tumor that is difficult
to treat and often fatal.

4. Liver function is complex, and liver dysfunction affects all
body systems.
For this reason, the nurse must understand how the liver
functions and must have expert assessment and clinical
management skills to care for patients undergoing complex
diagnostic and treatment procedures.
The liver plays additional roles in detoxification of chemicals
and synthesis and storage of important nutrients and The
liver is especially important in the regulation of glucose and
protein metabolism .

6. Functions of the liver include:
1. Storage of vitamins A, B, D; iron; and copper.
2. Synthesis of plasma proteins, including albumin and globulins.
3. Synthesis of the clotting factors vitamin K and prothrombin.
4.Storage of glycogen and synthesis of glucose from other
nutrients (gluconeogenesis).
5. Breakdown of fatty acids for energy.
6.Production of bile.
7. Detoxification and excretion of waste products.

7. FUNCTIONS OF THE LIVER
1. Glucose Metabolism : The liver plays a major role in
the metabolism of glucose and the regulation of blood
glucose concentration. After a meal, glucose is taken up
from the portal venous blood by the liver and converted
into glycogen, which is stored in the hepatocytes.

8. The liver also plays an important role in protein metabolism.
It synthesizes almost all of the plasma proteins (except
gamma globulin), including albumin, alpha and beta
globulins, blood clotting factors, specific transport proteins,
and most of the plasma lipoproteins.
Vitamin K is required by the liver for synthesis of
prothrombin and some of the other clotting factors.

9. The liver is also active in fat metabolism.
Fatty acids can be broken down for the production of
energy and the production of ketone bodies
(acetoacetic acid, beta-hydroxybutyric acid, and
acetone).

10. Vitamin and Iron Storage
Vitamins A, B, and D and several of the B-complex
vitamins are stored in large amounts in the liver.
Certain substances, such as iron and copper, are also
stored in the liver.

11. Drug Metabolism
The liver metabolizes many medications, such as
barbiturates, opioids, sedative agents, anesthetics,
and amphetamines.

12. Bile Formation
Bile is continuously formed by the hepatocytes and
collected in the canaliculi and bile ducts.
It is composed mainly of water and electrolytes such
as sodium, potassium, calcium, chloride, and
bicarbonate, and it also contains significant amounts
of lecithin, fatty acids, cholesterol, bilirubin, and bile
salts.

13. Bilirubin Excretion
Bilirubin is a pigment derived from the breakdown of
hemoglobin by cells of the reticuloendothelial
system, including the Kupffer cells of the liver.

14. ANATOMY OF THE LIVER
The liver is located behind the ribs in the upper right portion
of the abdominal cavity. It weighs about 1,500 g and is
divided into four lobes.

15. ANATOMY OF THE LIVER

16. ANATOMY OF THE LIVER

17. ASSESSMENT
1. HEALTH HISTORY
1. If liver function test results are abnormal, the patient may need to be
evaluated for liver disease.
In such cases, the health history will focus on exposure of the patient to
hepatotoxic substances or infectious agents.
2. The patient’s occupational, recreational, and travel history may assist
in identifying exposure to hepatotoxins (e.g., industrial chemicals, other
toxins) responsible for illness.
The patient’s history of alcohol and drug use, including but not limited
to the use of injectable drugs, provides additional information about
exposure to toxins and infectious agents.

18. ASSESSMENT
1. HEALTH HISTORY
3. A careful medication history to assess hepatic dysfunction
should address all prescribed and over-the counter
medications, herbal remedies, and dietary supplements used
by the patient currently and in the past.
4. Lifestyle behaviors that increase the risk for exposure to
infectious agents are identified.
5. Injectable drug use, sexual practices, and a history of
foreign travel are all potential risk factors for liver disease. The
amount , duration and type of alcohol consumption.

19. ASSESSMENT
1. HEALTH HISTORY
5. The family history includes questions about familial
liver disorders that may have their etiology in alcohol
abuse or gallstone disease, as well as other familial or
genetic diseases, such as hemochromatosis, Wilson’s
disease, or alpha-1 antitrypsin disease.

20. ASSESSMENT
1. HEALTH HISTORY
6. The history also includes reviewing symptoms that suggest
liver disease such as .
1.Jaundice
2.Malaise and weakness fatigue
3. Pruritus
4. Abdominal pain, fever and anorexia.

21. ASSESSMENT
1. HEALTH HISTORY
5. Weight gain, edema and increasing abdominal girth.
6. Hematemesis, melena, hematochezia (passage of bloody
stools).
7. Easy bruising, decreased libido in men and secondary
amenorrhea in women, changes.
8. Changes in mental acuity, personality changes, and sleep
disturbances.

22. PHYSICAL EXAMINATION
1. The nurse assesses the patient for physical signs that may
occur with liver dysfunction, including pallor of chronic
illness and jaundice.
2. The skin, mucosa, and sclerae are inspected for jaundice,
and the extremities are assessed for muscle atrophy,
edema, and skin excoriation secondary to scratching.
3. The nurse observes the skin for petechiae or ecchymotic
areas (bruises), spider angiomas, and palmar erythema.

23. PHYSICAL EXAMINATION
1. The male patient is assessed for unilateral or bilateral
gynecomastia and testicular atrophy due to endocrine
changes.
2. The patient’s cognitive status (recall, memory, abstract
thinking) and neurologic status are assessed. The nurse
observes for general tremor, asterixis, weakness, and
slurred speech.

24. PHYSICAL EXAMINATION
1. The nurse assesses the abdomen for dilated
abdominal wall veins, ascites, and a fluid wave
(discussed later).
2. The abdomen is palpated to assess liver size and to
detect any tenderness over the liver.

25. Methods for Palpating the Liver

26. PHYSICAL EXAMINATION
Tenderness of the liver implies recent acute
enlargement with consequent stretching of the liver
capsule. The absence of tenderness may imply that
the enlargement is of long-standing duration.

27. Common clinical manifestations of Hepatic Dysfunction
1. Jaundice, resulting from increased bilirubin concentration in the blood
2. Portal hypertension, ascites, and varices, resulting from circulatory
changes within the diseased liver and producing severe GI hemorrhages
and marked sodium and fluid retention
3. Nutritional deficiencies, which result from the inability of the damaged
liver cells to metabolize certain vitamins; responsible for impaired
functioning of the central and peripheral nervous systems and for
abnormal bleeding tendencies
4. Hepatic encephalopathy or coma, reflecting accumulation of ammonia
in the serum due to impaired protein metabolism by the diseased liver.

28. Diagnostic Evaluation
1. LIVER FUNCTION TESTS: More than 70% of the
parenchyma of the liver may be damaged before liver
function test results become abnormal.
Function is generally measured in terms of serum enzyme
activity (i.e., alkaline phosphatase, lactic dehydrogenase,
serum aminotransferases) and serum concentrations of
proteins (albumin and globulins), bilirubin, ammonia,
clotting factors, and lipids.

29. LIVER FUNCTION TESTS
1. Serum aminotransferases (also called transaminases) are sensitive
indicators of injury to the liver cells and are useful in detecting acute liver
disease such as hepatitis.
2. Alanine aminotransferase (ALT) (formerly called serum glutamic-
pyruvic transaminase [SGPT]), aspartate aminotransferase (AST)
(formerly called serum glutamic-oxaloacetic transaminase [SGOT]), and
gamma glutamyl transferase (GGT) (also called G-glutamyl
transpeptidase) are the most frequently used tests of liver damage.
3. ALT levels increase primarily in liver disorders and may be used to
monitor the course of hepatitis or cirrhosis or the effects of treatments
that may be toxic to the liver.

30. LIVER BIOPSY

31. LIVER BIOPSY
1. Liver biopsy is the removal of a small amount of
liver tissue, usually through needle aspiration. It
permits examination of liver cells.
2. The most common indication is to evaluate diffuse
disorders of the parenchyma and to diagnose space-
occupying lesions. Liver biopsy is especially useful
when clinical findings and laboratory tests are not
diagnostic of liver disease.

32. Liver biopsy procedure

33. PRE PROCEDURE
1. Ascertain that results of coagulation tests (prothrombin time, partial
thromboplastin time, and platelet count) are available and that compatible donor
blood is available.
2. Check for signed consent; confirm that informed consent has been provided.
3. Measure and record the patient’s pulse, respirations, and blood pressure
immediately before biopsy.
4. Describe to the patient in advance: steps of the procedure; sensations expected;
after-effects anticipated; restrictions of activity and monitoring procedures to
follow.
5. Bleeding and bile peritonitis after liver biopsy are the major complications;
therefore, coagulation studies are obtained, their values are noted, and abnormal
results are treated before liver biopsy is performed.

34. POST PROCEDURE
1. Immediately after the biopsy, assist the patient to turn onto the right
side; place a pillow under the costal margin, and caution the patient to
remain in this position, recumbent and immobile, for several hours.
Instruct the patient to avoid coughing or straining.
2. Measure and record the patient’s pulse, respiratory rate, and blood
pressure at 10- to 15-minute intervals for the first hour, then every 30
minutes for the next 1 to 2 hours or until the patient’s condition
stabilizes.
3. If the patient is discharged after the procedure, instruct the patient to
avoid heavy lifting and strenuous activity for 1 week.

35. OTHER DIAGNOSTIC TESTS
1. Ultrasonography, computed tomography (CT), and magnetic resonance
imaging (MRI) are used to identify normal structures and abnormalities of the
liver and biliary tree.
2. A radioisotope liver scan may be performed to assess liver size and hepatic
blood flow and obstruction.
3. Laparoscopy (insertion of a fiber-optic endoscope through a small
abdominal incision) is used to examine the liver and other pelvic structures.
It is also used to perform guided liver biopsy, to determine the etiology of
ascites, and to diagnose and stage tumors of the liver and other abdominal
organs.

36. OTHER DIAGNOSTIC TESTS
1. Endoscopic Retrograde Cholangiopancreatography (ERCP) : Endoscopic
visualization of the common bile, pancreatic, and hepatic ducts with a flexible
fiber-optic endoscope inserted into the esophagus, passed through the
stomach and into the duodenum.

37. JAUNDICE

38. JAUNDICE
When the bilirubin concentration in the blood is
abnormally elevated, all the body tissues, including the
sclera and the skin, become yellow-tinged or greenish-
yellow, a condition called jaundice.
Jaundice becomes clinically evident when the serum
bilirubin level exceeds 2.5 mg/dL (43 fmol/L).

39. Types of Jaundice
There are several types of jaundice: hemolytic,
hepatocellular, obstructive, or jaundice due to
hereditary hyperbilirubinemia.
Hepatocellular and obstructive jaundice are the two
types commonly associated with liver disease.

40. Hemolytic Jaundice ( Prehepatic jaundice)
Hemolytic jaundice is the result of an increased
destruction of the red blood cells, the effect of which is to
flood the plasma with bilirubin so rapidly that the liver,
although functioning normally, cannot excrete the
bilirubin as quickly as it is formed.
This type of jaundice is encountered in patients with
hemolytic transfusion reactions and other hemolytic
disorders.

42. Hemolytic Jaundice ( Prehepatic jaundice)
Hemolytic jaundice is due to excessive break down of Red
blood cells.
Causes
1. Sickle cell anemia
2. Malaria
3. Thalassemia
4.Auto immune disorders
5.Massive hemorrhage

43. Hepatocellular Jaundice ( Hepatic jaundice)
Hepatocellular jaundice is caused by the inability of damaged
liver cells to clear normal amounts of bilirubin from the blood.
The causes of hepatocellular jaundice such as:
1. The cellular damage may be from infection, such as in viral hepatitis
(e.g., hepatitis A, B, C, D, or E) or other viruses that affect the liver (e.g.,
yellow fever virus, Epstein-Barr virus).
2. Medication or chemical toxicity (e.g., carbon tetrachloride, chloroform,
phosphorus, arsenicals, certain medications).
3. From alcohol consumption.

45. Hepatocellular Jaundice ( Hepatic jaundice)
Patients with hepatocellular jaundice may be mildly or severely
ill, with lack of appetite, nausea, malaise, fatigue, weakness,
and possible weight loss.
The serum bilirubin concentration and urine urobilinogen level
may be elevated.
In addition, AST and ALT levels may be increased, indicating
cellular necrosis.
The patient may report headache, chills, and fever if the cause
is infectious. Depending on the cause and extent of the liver cell
damage, hepatocellular jaundice may or may not be completely
reversible.

46. Obstructive Jaundice
Obstructive jaundice is a particular type of jaundice and occurs
when the essential flow of bile to the intestine is blocked and
remains in the bloodstream.
Obstructive jaundice of the extra hepatic type may be caused by
occlusion of the bile duct by a gallstone, an inflammatory
process, a tumor, or pressure from an enlarged organ.

49. Hereditary Hyperbilirubinemia
Hereditary Hyperbilirubinemia : Increased serum bilirubin levels
(hyperbilirubinemia) resulting from several inherited disorders can also produce
jaundice.
Gilbert’s syndrome is a familial disorder characterized by an increased level of
unconjugated bilirubin that causes jaundice.
Although serum bilirubin levels are increased, liver histology and liver function
test results are normal, and there is no hemolysis. This syndrome affects 2% to
5% of the population.
Other conditions that are probably caused by inborn errors of biliary metabolism
include Dubin–Johnson syndrome (chronic idiopathic jaundice, with pigment in
the liver) and Rotor’s syndrome (chronic familial conjugated hyperbilirubinemia
without pigment in the liver); “benign” cholestatic jaundice of pregnancy, with
retention of conjugated bilirubin.

52. Cirrhosis is a chronic disease
characterized by replacement of normal
liver tissue with diffuse fibrosis that
disrupts the structure and function of the
liver. There are three types of cirrhosis or
scarring of the liver.

53. HEPATIC CIRRHOSIS OR LIVER CIRRHOSIS
HEPATIC CIRRHOSIS or Cirrhosis of the liver is
characterized by scarring. It is a chronic disease in
which there has been diffuse destruction and fibrotic
regeneration of hepatic cells.

55. Types of liver cirrhosis
There are three types of cirrhosis or scarring of the liver:
1. Alcoholic cirrhosis, in which the scar tissue characteristically
surrounds the portal areas. This is most frequently due to chronic
alcoholism and is the most common type of cirrhosis.
2. Postnecrotic cirrhosis, in which there are broad bands of scar
tissue as a late result of a previous bout of acute viral hepatitis.
3. Biliary cirrhosis, in which scarring occurs in the liver around the
bile ducts. This type usually is the result of chronic biliary
obstruction and infection (cholangitis); it is much less common
than the other two types.

56. Clinical manifestations
Onset is insidious; may take years to develop.
Clinical manifestations include intermittent jaundice and fever. Initially
the liver is enlarged, hard, and irregular, but eventually it atrophies.
Early complaints include fatigue, anorexia, ankle edema in the
evening, epistaxis and bleeding gums, and weight loss.
A) Chronic dyspepsia, constipation, or diarrhea.
B) Plasma albumin is reduced, leading to edema and contributing to
ascites.
C) Anemia and poor nutrition lead to fatigue and weakness, wasting,
and depression.

57. Clinical manifestations
D) Deterioration of mental function from lethargy to delirium to
coma and eventual death.(Additional include deterioration of mental
function with impending hepatic encephalopathy and hepatic coma)
E) Estrogen-androgen imbalance causes spider angiomata and
palmar erythema; menstrual irregularities in females; testicular and
prostatic atrophy, gynecomastia, loss of libido, and impotence in
males.
F) VITAMIN DEFICIENCY AND ANEMIA (Because of inadequate
formation, use, and storage of certain vitamins (notably vitamins A, C,
and K), signs of their deficiency are common, particularly hemorrhagic
phenomena associated with vitamin K deficiency).

58. Clinical manifestations
Compensated Decompensated
Intermittent mild fever Ascites Jaundice
Vascular spiders Weakness, Muscle wasting and
Weight loss
Palmar erythema (reddened palms)
and Unexplained epistaxis
Continuous mild fever, Clubbing of
fingers
Ankle edema Purpura (due to decreased platelet
count) Spontaneous bruising
Vague morning indigestion ,Flatulent
dyspepsia and abdominal pain
Epistaxis Hypotension
Firm, enlarged liver Sparse body hair and White nails
Splenomegaly Gonadal atrophy

59. Assessment and Diagnostic Findings
The extent of liver disease and the type of treatment are determined after
reviewing the laboratory findings.
1. History collection .
2. Liver biopsy detects destruction and fibrosis of hepatic tissue.
3. Liver scan shows abnormal thickening and a liver mass.
4. CT scan determines the size of the liver and its irregular nodular surface.
5. Esophagoscopy to determine esophageal varices.
6. Paracentesis to examine ascitic fluid for cell, protein, and bacterial counts.
7. Laparoscopy and liver biopsy permit direct visualization of the liver.
8. Serum liver function test results are elevated.

60. Medical Management clients with liver cirrhosis
The management of the patient with cirrhosis is usually based on the
presenting symptoms. For example, antacids are prescribed to
decrease gastric distress and minimize the possibility of GI bleeding.
Vitamins and nutritional supplements promote healing of damaged
liver cells and improve the general nutritional status.
Minimize further deterioration of liver function through the
withdrawal of toxic substances, alcohol, and drugs.
Correction of nutritional deficiencies with vitamins and nutritional
supplements and a high-calorie and moderate- to high-protein diet.

61. Medical Management clients with liver cirrhosis
Treatment of ascites and fluid and electrolyte imbalances.
◦ Restrict sodium and water intake, depending on amount of fluid
retention.
◦ Bed rest to aid in diuresis.
◦ Diuretic therapy, frequently with spironolactone (Aldactone), a
potassium-sparing diuretic
◦ Abdominal paracentesis to remove fluid and relieve symptoms
◦ Administration of albumin to maintain osmotic pressure.

62. Medical Management clients with liver cirrhosis
Preliminary studies indicate that colchicine, an anti-inflammatory
agent used to treat the symptoms of gout, may increase the length of
survival in patients with mild to moderate cirrhosis.
Improved survival has been observed in patients with alcoholic
cirrhosis.
Colchicine is believed to reverse the fibrotic processes in cirrhosis,
and this has improved survival.

63. Colchicine

64. NURSING PROCESS: THE PATIENT WITH HEPATIC CIRRHOSIS
Assessment: Nursing assessment focuses on the onset of
symptoms and the history of precipitating factors,
particularly long-term alcohol abuse, as well as dietary
intake and changes in the patient’s physical and mental
status.
The patient’s past and current patterns of alcohol use
(duration and amount) are assessed and documented.
It is also important to document any exposure to toxic
agents encountered in the workplace or during recreational
activities.

65. NURSING PROCESS: THE PATIENT WITH HEPATIC CIRRHOSIS
3. The nurse assesses the patient’s mental status through
the interview and other interactions with the patient;
orientation to person, place, and time is noted.
4. The nurse assesses nutritional status, which is of major
importance in cirrhosis, by daily weights and monitoring of
plasma proteins, transferrin, and creatinine levels.

66. Complications
1. Bleeding and hemorrhage
2. Hepatic encephalopathy (Hepatic encephalopathy
and coma, possible complications of cirrhosis, may
present as deteriorating mental status and dementia
as well as physical signs such as abnormal voluntary
and involuntary movements).
3. Fluid volume excess

67. NURSING DIAGNOSES
1. Activity intolerance related to fatigue, general debility, muscle wasting, and
discomfort.
2. Imbalanced nutrition, less than body requirements, related to chronic gastritis,
decreased GI motility, and anorexia.
3. Impaired skin integrity related to compromised immunologic status, edema, and
poor nutrition.
4. Risk for injury and bleeding related to altered clotting mechanisms.
5. Disturbed Thought Processes related to deterioration of liver function and
increased serum ammonia level.
6. Imbalanced Nutrition: Less Than Body Requirements related to anorexia and GI
disturbances
7. Impaired Skin Integrity related to edema, jaundice, and compromised immunologic
status

68. Nursing Interventions
1. PROMOTING REST
2. IMPROVING NUTRITIONAL STATUS
3. PROVIDING SKIN CARE (Providing careful skin care is important because of
subcutaneous edema, the patient’s immobility, jaundice, and increased
susceptibility to skin breakdown and infection. Frequent position changes are
necessary to prevent pressure ulcers).
4. REDUCING RISK OF INJURY (The nurse protects the patient with cirrhosis
from falls and other injuries. The side rails should be in place and padded with
blankets in case the patient becomes agitated or restless. )
5. MONITORING AND MANAGING POTENTIAL COMPLICATIONS

69. Patient Education and Health Maintenance
1. Stress the necessity of giving up alcohol completely.
2. Urge acceptance of assistance from a substance abuse program.
3. Provide written dietary instructions.
4. Encourage daily weighing for self-monitoring of fluid retention or depletion.
5. Discuss adverse effects of diuretic therapy.
6. Emphasize the importance of rest, a sensible lifestyle, and an adequate, well-
balanced diet.
7. Involve the person closest to the patient because recovery usually is not easy
and relapses are common.
8. Stress the importance of continued follow-up for laboratory tests and
evaluation by a health care provider.

71. PORTAL HYPERTENSION
Portal hypertension is abnormally high blood pressure in
the portal vein (the large vein that brings blood from the
intestine to the liver) and its branches.
Obstructed blood flow through the damaged liver results in
increased blood pressure (portal hypertension) throughout
the portal venous system.
Although portal hypertension is commonly associated with
hepatic cirrhosis, it can also occur with non cirrhotic liver
disease.

72. Portal hypertension is defined as the elevation of
the hepatic venous pressure gradient to > 5 mmhg.

75. ASCITES

76. ASCITES
Ascites is of Greek derivation ("askos") and refers to a bag
or sack and describes pathologic fluid accumulation within
the peritoneal cavity.
Most patients (85%) with ascites have cirrhosis.

77. Peritoneal cavity It is a potential space between the parietal
peritoneum and visceral peritoneum, the two membranes separate
the organs in the abdominal cavity from the abdominal wall.

78. Peritoneal fluid It is a normal, lubricating fluid found in the peritoneal
cavity.
The fluid is mostly water with electrolytes, antibodies, white blood
cells, albumin, glucose and other biochemical.
Reduce the friction between the abdominal organs as they move
around during digestion.

79. Ascites is defined as the accumulation fluid in the
peritoneal cavity ( abdominal cavity).

80. Pathophysiology
The mechanisms responsible for the development of ascites are not
completely understood.
Portal hypertension and the resulting increase in capillary pressure
and obstruction of venous blood flow through the damaged liver
are contributing factors.
The failure of the liver to metabolize aldosterone increases sodium
and water retention by the kidney.
Sodium and water retention, increased intravascular fluid volume,
and decreased synthesis of albumin by the damaged liver all
contribute to fluid moving from the vascular system into the
peritoneal space.

82. Clinical Manifestations
1. Increased abdominal girth and rapid weight gain
are common presenting symptoms of ascites.
2. The patient may be short of breath and
uncomfortable from the enlarged abdomen, and
striae and distended veins may be visible over the
abdominal wall.
3. Fluid and electrolyte imbalances are common.

84. Assessment and Diagnostic Evaluation
The presence and extent of ascites are assessed by
percussion of the abdomen. When fluid has
accumulated in the peritoneal cavity, the flanks bulge
when the patient assumes a supine position.
The presence of fluid can be confirmed either by
percussing for shifting dullness or by detecting a fluid
wave.

86. Medical Management
1. DIETARY MODIFICATION : The goal of treatment
for the patient with ascites is a negative sodium
balance to reduce fluid retention. Table salt, salty
foods, salted butter and margarine, and all ordinary
canned and frozen foods (foods that are not
specifically prepared for low-sodium diets) should be
avoided.

87. Medical Management
2. DIURETICS: Use of diuretics along with sodium restriction
is successful in 90% of patients with ascites.
Spironolactone (Aldactone), an aldosteroneblocking agent, is
most often the first-line therapy in patients with ascites from
cirrhosis.
Possible complications of diuretic therapy include fluid and
electrolyte disturbances (including hypovolemia,
hypokalemia, hyponatremia, and hypochloremic alkalosis)
and encephalopathy.

88. Medical Management
PARACENTESIS : Paracentesis is the removal of fluid (ascites)
from the peritoneal cavity through a small surgical incision or
puncture made through the abdominal wall under sterile
conditions.

89. PARACENTESIS
Paracentesis was once considered a routine form of
treatment for ascites but is now performed primarily
for diagnostic examination of ascitic fluid, for
treatment of massive ascites that is resistant to
nutritional and diuretic therapy.

90. Abdominal Paracentesis

91. Abdominal Paracentesis

92. PREPROCEDURE
1. Prepare the patient by providing the necessary information and
instructions about the procedure and by offering reassurance.
2. Instruct the patient to void.
3. Gather appropriate sterile equipment and collection receptacles.
4. Place patient in upright position on edge of bed with feet
supported on stool, or place in chair. Fowler’s position should be
used for the patient confined to bed.
5. Place sphygmomanometer cuff around patient’s arm to allow
monitoring of blood pressure during the procedure.

93. PROCEDURE
1. The physician, using aseptic technique, inserts the trocar
through a puncture wound below the umbilicus.
2. Help the patient maintain position throughout
procedure.
3. Measure and record blood pressure at frequent intervals
from the beginning of the procedure.
4. Monitor the patient closely for signs of vascular collapse:
pallor, increased pulse rate, or decreased blood pressure.

94. POST PROCEDURE
1. Return patient to bed or to a comfortable sitting
position.
2. Measure, describe, and record the fluid collected.
3. Label samples of fluid and send to laboratory.
4. Continue to monitor vital signs every 15 minutes for 1
hour, every 30 minutes over 2 hours, then every hour over 2
hours and then every 4 hours. Monitor temperature after
procedure and every 4 hours.

95. POST PROCEDURE
5. Assess for hypovolemia, electrolyte loss, changes in
mental status, and encephalopathy.
6. Check puncture site when taking vital signs for bleeding
and leakage.
7. Provide patient education (especially if patient is
discharged after procedure) regarding monitoring for
bleeding or excess drainage from puncture site, avoiding
heavy lifting or straining, changing position slowly, and
monitoring for fever.

96. Nursing Management
If a patient with ascites from liver dysfunction is
hospitalized, nursing measures include assessment
and documentation of intake and output, abdominal
girth, and daily weight to assess fluid status.
The nurse monitors serum ammonia and electrolyte
levels to assess electrolyte balance, response to
therapy, and indicators of encephalopathy.

97. HEPATIC ENCEPHALOPATHY & COMA
The loss of brain function when a damaged liver
doesn't remove toxins from the blood.
Hepatic encephalopathy, a life-threatening
complication of liver disease, occurs with profound
liver failure and may result from the accumulation of
ammonia and other toxic metabolites in the blood.

98. HEPATIC ENCEPHALOPATHY & COMA
Hepatic coma represents the most advanced stage of
hepatic encephalopathy. Some researchers describe a
false or weak neurotransmitter as a cause, but the
exact mechanism is not fully understood.

99. Pathophysiology
1. Ammonia accumulates because damaged liver cells fail to
detoxify and convert to urea the ammonia that is constantly
entering the bloodstream.
2. Ammonia enters the bloodstream as a result of its
absorption from the GI tract and its liberation from kidney
and muscle cells.
The increased ammonia concentration in the blood causes
brain dysfunction and damage, resulting in hepatic
encephalopathy

100. Pathophysiology
1. Other factors unrelated to increased serum ammonia
levels that may cause hepatic encephalopathy in susceptible
patients include excessive diuresis, dehydration, infections,
surgery, fever, and some medications (sedative agents,
tranquilizers, analgesic agents, and diuretic medications that
cause potassium loss).

103. Clinical Manifestations
1. The earliest symptoms of hepatic encephalopathy include
minor mental changes and motor disturbances.
2. The patient appears slightly confused, has alterations in
mood, becomes unkempt, and has altered sleep patterns.
3. The patient tends to sleep during the day and have
restlessness and insomnia at night. As hepatic
encephalopathy progresses, the patient may be difficult to
awaken.

104. Clinical Manifestations
1. Asterixis ( flapping tremor of the hands)
(Asterixis (also called the flapping tremor, or liver flap) is a
tremor of the hand when the wrist is extended, sometimes
said to resemble a bird flapping its wings.) may occur.
Simple tasks, such as handwriting, become difficult.
A handwriting or drawing sample (e.g., star figure), taken
daily, may provide graphic evidence of progression or
reversal of hepatic encephalopathy. Inability to reproduce a
simple is referred to asconstructional apraxia

105. Asterixis ( flapping tremor of the hands

106. Assessment and Diagnostic Findings
1. The electroencephalogram (EEG)
2. Occasionally, fetor hepaticus, a sweet, slightly fecal
odor to the breath presumed to be of intestinal origin
may be noticed.
Approximately 35% of all patients with cirrhosis of
the liver die in hepatic coma.

107. Medical Management
Lactulose (Cephulac) is administered to reduce serum ammonia
levels. It acts by several mechanisms that promote the excretion of
ammonia in the stool:

108. Medical Management
Possible side effects include intestinal bloating and cramps, which
usually disappear within a week. To mask the sweet taste, to which
some patients object, lactulose can be diluted with fruit juice.
The patient is closely monitored for hypokalemia and dehydration.
Other laxatives are not prescribed during lactulose administration
because their effects would disturb dosage regulation.
Lactulose can be administered by nasogastric tube or enema for
patients who are comatose or in whom oral administration is
contraindicated or impossible.

109. Medical Management
Other aspects of management include intravenous
administration of glucose to minimize protein breakdown,
administration of vitamins to correct deficiencies, and
correction of electrolyte imbalances (especially potassium).
NURSING ALERT (The patient receiving lactulose is
monitored closely for the development of watery diarrheal
stools, because they ! indicate a medication overdose)

110. Additional principles of management of hepatic
encephalopathy include the following
1. Therapy is directed toward treating or removing the cause.
2. Neurologic status is assessed frequently. A daily record is kept of
handwriting and performance in arithmetic to monitor mental status.
3. Fluid intake and output and body weight are recorded each day.
4. Vital signs are measured and recorded every 4 hours.
5. Potential sites of infection (peritoneum, lungs) are assessed
frequently, and abnormal findings are reported promptly.
6. Serum ammonia level is monitored daily.

111. 7. Protein intake is restricted in patients who are comatose or who have
encephalopathy that is refractory to lactulose and antibiotic therapy.
8. Reduction in the absorption of ammonia from the GI tract is accomplished by
the use of gastric suction, enemas, or oral antibiotics.
9. Electrolyte status is monitored and corrected if abnormal.
10. Sedatives, tranquilizers, and analgesic medications are discontinued.
11. Benzodiazepine antagonists (flumazenil [Romazicon]) may be administered
to improve encephalopathy whether or not the patient has previously taken
benzodiazepines.

112. Nutritional Management of Hepatic Encephalopathy
1. Prevent the formation and absorption of toxins, principally ammonia, from the
intestine.
2. Keep daily protein intake between 1.0 and 1.5 g/kg, depending on the degree of
decompensation.
3. Avoid protein restriction if possible, even in those with encephalopathy. If necessary,
implement temporary restriction of 0.5 g/kg.
4. For patients who are truly protein-intolerant, provide additional nitrogen in the form
of an amino acid supplement. Use of branched-chain amino acids is still controversial.
5. Provide small, frequent meals and an evening snack of complex carbohydrates to avoid
protein loading.
6. Substitute vegetable protein for animal protein in as high a percentage as possible.

113. Nursing Management
The nurse is responsible for maintaining a safe environment to
prevent injury, bleeding, and infection.
The nurse administers the prescribed treatments and monitors the
patient for the many potential complications.
The nurse also communicates with the patient’s family to keep
them informed about the patient’s status, and supports them by
explaining the procedures and treatments that are part of the
patient’s care.

114. Hepatocellular Carcinoma (Liver Cancer) Hepatic
tumors may be malignant or benign. Benign liver
tumors.

115. What is Hepatocellular Carcinoma?
1. Most primary liver cancers are classified as hepatocellular
carcinoma.
2. Hepatocellular carcinoma is a malignant tumor composed of cells
resembling hepatocytes ; however, the resemblance varies with the
degree of differentiation .
3. Hepatocellular carcinoma is commonly associated with cirrhosis
This type of liver cancer is potentially curable by surgical resection.
However, only those patients with localized disease are surgical
candidates.

116. Most primary liver tumours (90%) originate in
the parenchymal cells and are hepatomas ( also
called hepatocellular carcinomas).

117. Pathophysiology and Etiology
1. Incidence of primary cancer of the liver is increasing in the United
States in the younger population and in females.
2. Cirrhosis, HBV, and HCV have been implicated in its etiology.
3. Rarer associated causes are hemachromatosis; alpha1-antitrypsin
deficiency; aflatoxins; chemical toxins, such as vinyl chloride and
Thorotrast; carcinogens in herbal medicines; nitrosamines; and
ingestion of hormones, as in oral contraceptives.
4. Few cancers originate in the liver. Primary liver tumors usually are
associated with chronic liver disease, hepatitis B and C infections, and
cirrhosis.

118. LIVER METASTASES
Metastases from other primary sites are found in the
liver in about half of all advanced cancer cases (Bacon
& Di Bisceglie, 2000).
Malignant tumors are likely to reach the liver
eventually, by way of the portal system or lymphatic
channels, or by direct extension from an abdominal
tumor.

119. Clinical Manifestations
1. The early manifestations of malignancy of the liver include
pain, a continuous dull ache in the right upper quadrant,
epigastrium, or back.
2. Weight loss, loss of strength, anorexia, and anemia may
also occur. The liver may be enlarged and irregular on
palpation.
3. With portal vein obstruction, ascites and esophageal
varices occurs.

120. Assessment and Diagnostic Findings
1. The liver cancer diagnosis is based on clinical signs and symptoms, the
history and physical examination, and the results of laboratory and x-ray
studies.
2. Increased serum levels of bilirubin, alkaline phosphatase, AST, GGT, and
lactic dehydrogenase may occur.
3. AFP (alpha-fetoprotein) is the principal tumor marker for hepatocellular
carcinoma and is elevated in 70% to 95% of patients with primary liver cancer.
4. Ultrasonography and CT along with MRI are the most useful noninvasive
tests to detect liver cancer and assess if the tumor can be surgically removed.
5. Percutaneous liver needle biopsy or biopsy assisted by ultrasonography or
CT scan may be done.
6. Laparoscopy with liver biopsy may be performed.

121. 1. Liver function test
2. Laboratory investigation of Alpha- fetoprotein
levels increase above 500 mcg/ml.

122. Medical Management
Although surgical resection of the liver tumor is possible in
some patients, the underlying cirrhosis, so prevalent in cancer
of the liver, increases the risks associated with surgery.
Radiation therapy and chemotherapy have been used in
treating cancer of the liver with varying degrees of success.
Although these therapies may prolong survival and improve
quality of life by reducing pain and discomfort, their major
effect is palliative.

123. Medical Management
PERCUTANEOUS BILIARY DRAINAGE (PBD) :
Percutaneous biliary or transhepatic drainage is used to
bypass biliary ducts obstructed by liver, pancreatic, or bile
duct tumors in patients with inoperable tumors or in those
considered poor surgical risks.

124. PERCUTANEOUS BILIARY DRAINAGE (PBD)

125. OTHER NONSURGICAL TREATMENTS
Laser hyperthermia has been used to treat hepatic metastases. Heat
has been directed to tumors through several methods to cause
necrosis of the tumor cells while sparing normal tissue.

126. SURGICAL MANAGEMENT
1. Surgical resection is the treatment of choice when HCC is con- fined to one
lobe of the liver and the function of the remaining liver is considered adequate
for postoperative recovery.
2. In preparation for surgery, the patient’s nutritional, fluid, and general
physical status is assessed and efforts are undertaken to ensure the best
physical condition possible.
Support, explanation, and encouragement are provided to help the patient
prepare psychologically for the surgery.
3. Extensive diagnostic studies may be performed. Specific studies may include
liver scan, liver biopsy, cholangiography, selective hepatic angiography,
percutaneous needle biopsy, peritoneoscopy, laparoscopy, ultrasound, CT scans,
MRI, and blood tests, particularly determinations of serum alkaline
phosphatase, AST, and GGT and its isoenzymes.

127. Lobectomy (Removal of a lobe of the liver is the most
common surgical procedure for excising a liver tumor.

128. Cryosurgery
In cryosurgery (cryoablation), tumors are destroyed
by liquid nitrogen at −196° C. To destroy the diseased
tissue, two or three freeze-and-thaw cycles are
administered via probes during open laparotomy.

129. Liver transplantation (LT) is a life saving procedure for
patients with end stage liver disease and its complications,
and for liver failure.
LT is also curative for some hereditary metabolic disorders
like familial hypercholesterolemia and for selected cases of
malignancies involving the liver, such as hepatocellular
carcinoma (HCC) and hepatoblastoma.

130. Liver Transplantation
Removing the liver and replacing it with a healthy donor
organ is another way to treat liver cancer.
Recurrence of the primary liver malignancy after
transplantation, however, has been reported to occur in 70%
to 85% of cases, and the survival time after recurrence is
brief.
But transplant surgery is performed infrequently because of
its risks, its high cost, and the difficulty procuring organs.

131. Liver transplantation is used to treat life-threatening,
end-stage liver disease for which no other form of
treatment is available.
The transplantation procedure involves total removal
of the diseased liver and its replacement with a
healthy liver in the same anatomic location
(orthotopic liver transplantation [OLT]).

132. Liver Transplantation

133. Liver transplantation

134. Indications for Liver transplantation
General indications for liver transplantation include:
1. irreversible advanced chronic liver disease
2. fulminant hepatic failure
3. metabolic liver diseases, and some hepatic malignancies.
Examples of disorders that are indications for liver
transplantation include hepatocellular liver disease (e.g.,
viral hepatitis, drug- and alcohol-induced liver disease,
and Wilson’s disease) and cholestatic diseases (primary
biliary cirrhosis, sclerosing cholangitis, and biliary
atresia).

135. COMPLICATIONS
 The postoperative complication rate is high, primarily
because of technical complications or infection.
 Immediate postoperative complications may include
bleeding, infection, and rejection.
 Disruption, infection, or obstruction of the biliary
anastomosis and impaired biliary drainage may occur.
Vascular thrombosis and stenosis are other potential
complications.

136. Pre- Operative Nursing interventions
Care of the client undergoing liver transplantation involves
initiation of immunosuppression therapy (The definition of
induction therapy is intensive peri-operative prophylactic
immunosuppression used to prevent acute cellular
rejection in the first months following transplantation) and
pre – and post operative emotional support of patient and
family.

137. Pre-operative preparation
1. As ordered , begin immunosuppressant therapy to decrease the risk
of tissue rejection, using such drugs as cyclosporine, tacrolimus and
corticosteroids.
2. Explain the need for lifelong therapy to prevent rejection.
3. Before transplant surgery, address the patients ( and family
members) emotional needs.
4. The nurse and other health care team members provide the patient
and family with full explanations about the procedure, the chances of
success, and the risks, rejection of organ including the side effects of
long-term immunosuppression.
5. Malnutrition, massive ascites, and fluid and electrolyte
disturbances are treated before surgery to increase the chance of a
successful outcome.

138. POSTOPERATIVE NURSING INTERVENTIONS
1. The patient is maintained in an environment as free from bacteria,
viruses, and fungi as possible, because immunosuppressive
medications reduce the body’s natural defenses.
2. In the immediate postoperative period, cardiovascular, pulmonary,
renal, neurologic, and metabolic functions are monitored
continuously.
3. Mean arterial and pulmonary artery pressures are monitored
continuously.

139. 4. Cardiac output, central venous pressure, pulmonary
capillary wedge pressure, arterial and mixed venous blood
gases, oxygen saturation, oxygen demand and delivery, urine
output, heart rate, and blood pressure are used to evaluate the
patient’s hemodynamic status and intravascular fluid volume.
5. Liver function tests, electrolyte levels, the coagulation
profile, chest x-ray, electrocardiogram, and fluid output,
including urine, bile, and drainage from Jackson-Pratt tubes,
are monitored closely.

140. Post operative care
1. Maintaining immunosuppressant therapy.
2. Monitoring for early signs of rejection and other complications.
3. Prevent opportunistic infections, which can lead to rejection and providing
emotional support and reassurance throughout the prolonged recovery period.
4. Monitor vital signs every 15 minutes until stable, and monitor for haemorrhage
and rejection.
5. Perform hourly assessments of fluid volume and vital signs required to detect
bleeding and hypovolemic shock, along with pulses, urine output, LOC.
6. Assess incision site for signs symptoms of wound infection or abscess.
7. If the patient complains of acute pain in the right upper quadrant ( RUQ),
cramping pain or tenderness, N &V , he or she may be experiencing vascular
obstruction and need emergency thrombectomy.

141. 1. Assess the daily weight.
2. After removal of the endotracheal tube, the nurse
encourages the patient to use an incentive spirometer,
pulmonary hygiene protocol to decrease the risk for
atelectasis.
3. Once the arterial lines and the urinary catheter are
removed, the patient is assisted to get out of bed, to
ambulates tolerated, and to participate in self-care to
prevent the complications associated with immobility.

142. Patient Teaching
1. Before discharge the client teach the patient and family members to
recognize the early indicators of tissue rejection ( pain and tenderness
in the RUQ or centre of the back, fever tachycardia, jaundice and
changes in colour in urine and stool )
2. The nurse provides written as well as verbal instructions about how
and when to take the medications. To avoid running out of medication
or skipping a dose, the patient must make sure that an adequate
supply of medication is available.