ASSESSMENT

HEALTH HISTORY PHYSICAL ASSESSMENT

- If liver function test is abnormal the patient is - The nurse assesses the patient for physical signs that
evaluated for liver disease. may occur with liver dysfunction:
- Health history focuses on: o including the pallor often seen with chronic
o Exposure of the client to hepatoxic substances or illness and jaundice.
infectious agents o The skin, mucosa, and sclerae are inspected for
o Patients occupation, recreational, and travel jaundice, and the extremities are assessed for
history muscle atrophy, edema, and skin excoriation
Travel history may assist the patients secondary to scratching.
exposure to hepatoxins - The nurse observes the skin for petechiae or
o The patients history of alcohol and drug use ecchymotic areas (bruises), spider angiomas, and
o Lifestyles behaviors that increase the risk for palmar erythema.
exposure to infectious agents are identified. - The male patient is assessed for unilateral or bilateral
o Evaluation of the patients past medical history to gynecomastia and testicular atrophy due to hormonal
identify the risk factor for the development of liver changes.
disease - The patients cognitive status (recall, memory,
Current and past medical conditions abstract thinking) and neurologic status are
Physiological or psychiatric nature assessed.
- Family history - The nurse observes for:
o Question about familial liver: o general tremor
o Origin of alcohol abuse o asterixis
o Gallstone disease o weakness
o Genetic disease ( hematochromatosis, wilsons o slurred speech.
disease, antitrypsin disease ) - The nurse assesses for the presence:
- Symptoms that may have their origin in liver disease o of an abdominal fluid wave (discussed later).
but not specific to hepatic dysfunction include : o The abdomen is palpated to assess liver size and
o jaundice to detect any tenderness over the liver.
o malaise o The liver may be palpable in the right upper
o weakness quadrant.
o fatigue o A palpable liver presents as a firm, sharp ridge
o pruritus with a smooth surface
o abdominal pain - The nurse estimates the size of the liver by:
o fever o percussing its upper and lower borders.
o anorexia o If the liver is not palpable but tenderness is
o weight gain suspected, tapping the lower right thorax briskly
o edema may elicit tenderness.
o increasing abdominal girth o For comparison, the nurse then performs a
o hematemesis similar maneuver on the left lower thorax
o melena - If the liver is palpable, the examiner notes and
o hematochezia (passage of bloody stools) records:
o easy bruising o its size
o changes in mental acuity o its consistency
o personality changes o any tenderness
o sleep disturbances o whether its outline is regular or irregular
o decreased libido in men
o secondary amenorrhea in women.
- If the liver is enlarged the degree to which it descends
below the right costal margin is recorded to provide
some indication of its size.
- The examiner determines whether the livers:
o edge is sharp and smooth or blunt
o whether the enlarged liver is nodular or smooth.
- The liver of a patient with cirrhosis is:
o small and hard
- the liver of a patient with acute hepatitis:
o soft
o the hand easily moves the edge.
- The liver of a patient with viral hepatitis is:
o tender
- The liver of the patient that is alcoholic is not tender
DIAGNOSTIC EVALUATION
LIVER FUNCTION TEST
- 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:
o serum enzyme activity (ie, serum
aminotransferases, alkaline phosphatase, lactic
dehydrogenase)
o serum concentrations of proteins (albumin and
globulins), bilirubin, ammonia, clotting factors,
and lipids.
- These test may be helpful in assessing patients with
liver disease.
- the nature and extent of hepatic dysfunction cannot
be determined by these tests alone, because other
disorders can affect test results.
- Serum aminotransferases (previously called
transaminases)
o are sensitive indicators of injury to the liver cells
and are useful in detecting acute liver disease
such as hepatitis.
- Alanine aminotransferase (ALT),
- aspartate amino- transferase (AST),
- gamma-glutamyl transferase (GGT) (also called G-
glutamyl transpeptidase)
o are the most frequently used tests of liver
damage.
o 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.
LIVER BIOPSY
- Liver biopsy is the removal of a small amount of liver
tissue, usually through needle aspiration
- It permits examination of liver cells.
- 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.
- Liver biopsy can be performed percutaneously with
ultrasound guidance
- transvenously through the right internal jugular vein to
right hepatic vein under fluoroscopic control.
- Liver biopsy can also be performed laparoscopically.
MAJOR COMPLICATION
- Bleeding and bile peritonitis after liver biopsy
REMEDY
- coagulation studies are obtained,
- their values are noted
- abnormal results are treated before liver biopsy is
performed.
- Other techniques for liver biopsy are preferred if
ascites or coagulation abnormalities exist.
OTHER DIAGNOSTIC TEST
- Ultrasonography
- Computed Tomography (CT)
- magnetic resonance imaging (MRI) are used
o To identify normal structures and abnormalities
of the liver and biliary tree.
- Radioisotope Liver Scan
o To assess liver size and hepatic blood flow and
obstruction.
- Laparoscopy
o insertion of a fiberoptic endoscope through a
small abdominal incision
o Used to examine the liver and other pelvic
structures.
 o It is also used to perform guided liver biopsy
o To determine the cause of ascites
JAUNDICE
o To diagnose and stage tumors of the liver and
other abdominal organs. - When the bilirubin concentration in the blood is
abnormally elevated
- all the body tissues, including the sclerae and the
MANIFESTATIONS OF HEPATIC DYSFUNCTION skin, become tinged yellow or greenish yellow
- Jaundice becomes clinically evident when:
- Hepatic dysfunction results from damage to:
o the serum bilirubin level exceeds 2.5 mg/dL (43
o the livers parenchymal cells
fmol/L).
o directly from primary liver diseases
- Increased serum bilirubin levels and jaundice may
o indirectly from either obstruction of bile flow
result from:
o derangements of hepatic circulation
o impairment of hepatic uptake
o conjugation of bilirubin
o excretion of bilirubin into the biliary system.
- Liver dysfunction may be
o acute
o chronic
Several types of jaundice:
o the latter is far more common
- Chronic Liver Disease - hemolytic
o Disease processes that lead to hepatocellular - hepatocellular
dysfunction may be caused by infectious agents - obstructive jaundice
such as: - jaundice due to hereditary hyperbilirubinemia.
bacteria
viruses
anoxia Two types commonly associated with liver disease.
metabolic disorders
toxins - Hepatocellular jaundice
medications - obstructive jaundice
nutritional deficiencies
hypersensitivity states.
- Most common cause of parenchymal damage is HEMOLYTIC JAUNDICE
malnutrition, especially that related to alcoholism. - is the result of an increased destruction of the red
- Most common and significant manifestations blood cells, the effect of which is to flood the plasma
- of liver disease are : with bilirubin so rapidly that the liver
o jaundice - although functioning normally, cannot excrete the
o portal hypertension bilirubin as quickly as it is formed.
o ascites - encountered in patients with hemolytic transfusion
o varices reactions and other hemolytic disorders.
o nutritional deficiencies (resulting from the - the bilirubin in the blood is predominantly
inability of damaged liver cells to metabolize unconjugated or free.
certain vitamins) - Fecal and urine urobilinogen levels are increased, but
o hepatic encephalopathy or coma. the urine is free of bilirubin.
- consequences of liver disease are numerous and - do not experience symptoms or complications as a
varied. result of the jaundice per se.
- Their ultimate effects are often incapacitating or life- - However, prolonged jaundice, even if mild,
threatening predisposes to the formation of pigment stones in the
- their presence is ominous gallbladder, and extremely severe jaundice (levels of
- Treatment often is difficult. free bilirubin exceeding 20 to 25 mg/dL) poses a risk
for brainstem damage.
 - Depending on the cause and extent of the liver cell
damage
HEPATOCELLULAR JAUNDICE
- hepatocellular jaundice may be completely reversible.
- caused by the inability of damaged liver cells to clear
normal amounts of bilirubin from the blood.
- The cellular damage may be caused by: OBSTRUCTIVE JAUNDICE
o hepatitis viruses
- resulting from extrahepatic obstruction may be
o other viruses that affect the liver
caused by :
yellow fever virus
o occlusion of the bile duct from a gallstone
Epstein-Barr virus
o an inflammatory process
o medications or chemical toxins
o a tumor
carbon tetrachloride
o pressure from an enlarged organ (eg, liver,
chloroform
gallbladder).
phosphorus
- The obstruction may also involve the small bile ducts
arsenicals
within the liver (ie, intra- hepatic obstruction);
certain medications
- this may be caused by pressure on these channels
o alcohol.
from inflammatory swelling of the liver or by an
- Cirrhosis of the liver is a form of hepatocellular
inflammatory exudate within the ducts themselves.
disease that may produce jaundice. It is usually
- Intrahepatic obstruction resulting from stasis and
associated with excessive alcohol intake
inspissation (thickening) of bile within the canaliculi
- a late result of liver cell necrosis caused by viral
may occur after the ingestion of certain medications,
infection
which are referred to as cholestatic agents.
- In prolonged obstructive jaundice, cell damage
eventually develops, so that both types of jaundice Cholestatic agents
(ie, obstructive and hepatocellular jaundice) appear
together o phenothiazine
o antithyroid medications
o sulfonylureas
o tricyclic antidepressant agents
SIGN AND SYMPTOMS
o nitrofurantoin
- may be mildly or severely ill o androgens and estrogens
- with lack of appetite o propylthiouracil
- nausea o amoxicillin-clavulanic acid
- malaise o erythromycin estolate.
- fatigue - bile cannot flow normally into the intestine and
- weakness becomes backed up into the liver substance.
- possible weight loss. - It is then reabsorbed into the blood and carried
- In some cases of hepatocellular disease, throughout the entire body
- jaundice may not be obvious - staining the skin, mucous membranes, and sclerae.
- It is excreted in the urine, which becomes deep
orange and foamy.
FOR CELLULAR NECROSIS - Because of the decreased amount of bile in the
intestinal tract the stools become light or clay
- The serum bilirubin concentration and the urine colored.
urobilinogen level may be elevated. - The skin may itch intensely, requiring repeated
- In addition, AST and ALT levels may be increased soothing baths.
- patient may report : - Dyspepsia and intolerance to fatty foods may develop
o headache because of impaired fat digestion in the absence of
o chills intestinal bile.
o fever if the cause is infectious
HERERIDITARY HYPERBILIRUBINEMIA ASCITES

- Increased serum bilirubin levels (hyperbilirubinemia),

resulting from any of several inherited disorders
- Gilberts syndrome
o is a familial disorder characterized by an
increased level of unconjugated bilirubin
o serum bilirubin levels are increased
o liver histology and liver function test results are
normal
o there is no hemolysis.
o This syndrome affects 3% to 8% of the
population, predominantly males

OTHER CONDITIONS CAUSED BY INBORN ERRORS of

BILIARY METABOLISM:
CLINICAL MANIFESTATION
- Dubin-Johnson syndrome
- Increase abdominal girth
o chronic idiopathic jaundice, with pigment in the
- Rapid weight gain
liver
- Short of breath
- Rotors syndrome
- Uncomfortable from enlarged abdomen
o chronic familial conjugated hyperbilirubinemia,
- Striae
without pigment in the liver
- the benign cholestatic jaundice of pregnancy, with - Distended veins may be visble over abdominal wall
- Umbilical hernias(patient with cirrhosis)
retention of conjugated bilirubin, probably secondary
- Fluid and electrolyte imbalance
to unusual sensitivity to the hormones of pregnancy;
- benign recurrent intrahepatic cholestasis.

ASSESSMENT AND DIAGNOSTIC FINDINGS

PORTAL HYPOTENSION - Percussion of the abdomen
- the increased pressure throughout the portal venous
system that results from obstruction of blood flow
through the damaged liver.
- Commonly associated with hepatic cirhosis
- Also occur with non cirrhotic liver disease
- Although splenomegaly (enlarged spleen) with
possible hypersplenism is a common manifestation of
portal hypertension
- the two major consequences of portal hypertension
are:
o ascites
o varices
 - Dietary control of ascites via strict sodium restriction
is difficult to achieve at home.
- Non responders to this therapy may require diuretics
theraphy

Diuretics

- Spironolactone (Aldactone), an aldosterone blocking

- When fluid has accumulated in the peritoneal cavity,
the flanks bulge when the patient assumes a supine
position.
- presence of fluid can be confirmed either by
percussing for shifting dullness or by detecting a fluid
wave
- A fluid wave is likely to be found only if a large amount
of fluid is present.
- Daily measurement and recording of abdominal girth
and body weight are essential to assess the
progression of ascites and its response to treatment.
agent, is most often the first-line therapy in patients
with ascites from cirrhosis.
- Oral diuretics such as :
o furosemide (Lasix) may be added but should be
used cautiously, because longterm use may
induce severe sodium depletion (hyponatremia).
o Ammonium chloride and acetazolamide (Diamox)
are contraindicated because of the possibility of
precipitating hepatic coma.
- Daily weight loss should not exceed
o 1 to 2 kg (2.2 to 4.4 lb) in patients with ascites
and peripheral edema
o 0.5 to 0.75 kg (1.1 to 1.65 lb) in patients without
edema
- Fluid restriction is not attempted unless the serum
sodium concentration is very low.
POSSIBLE COMPLICATIONS

MEDICAL MANAGEMENT - fluid and electrolyte disturbances

- hypovolemia
Dietary modification - hypokalemia
- Goal of treatment: - hyponatremia
- negative sodium balance to reduce fluid retention. - hypochloremic alkalosis
- Encephalopathy
o may be precipitated by dehydration and
AVOID: hypovolemia.

- Table salts
- salty foods
- salted butter
- margarine BED REST
- all ordinary canned - bed rest may be a useful therapy, especially for
- frozen foods that are not specifically prepared for low- patients whose condition is refractory to diuretics.
sodium (2-g sodium) diets It takes 2 to 3 months for
the patients taste buds to adjust
- Commercial salt substitutes need to be approved by
PARACENTESIS
the physician
o because those that contain ammonia could - removal of fluid (ascites) from the peritoneal cavity
precipitate hepatic coma. through a puncture or a small surgical incision
through the abdominal wall under sterile conditions.

- Ultrasound guidance may be indicated in some
patients who are at high risk for:
- bleeding because of an abnormal coagulation profile
- those who have had previous abdominal surgery and
may have adhesions.
- was once considered a routine form of treatment for
ascites.
- Albumin infusions help to correct decreases in
effective arterial blood volume that lead to sodium
retention.
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
- Transjugular intrahepatic portosystemic shunt (TIPS)
is a method of treating ascites in which a cannula is
threaded into the portal vein by the transjugular route
- To reduce portal hypertension
- expandable stent is inserted to serve as an
intrahepatic shunt between the portal circulation and
the hepatic vein.
- TIPS is the treatment of choice for refractive ascites.
- It is extremely effective in decreasing sodium
retention, improving the renal response to diuretic
therapy, and preventing recurrence of fluid
accumulation.
OTHER METHODS OF TREATMENT
- For patients who are not candidates for liver
transplant because of:
o High complication
o High incidence of shunt failure
NURSING MANAGEMENT
- nursing measures include assessment and
documentation of :
o intake and output
o abdominal girth
o daily weight to assess fluid status.
- The nurse monitors serum ammonia and electrolyte
levels
o to assess electrolyte balance, response to
therapy, and indicators of encephalopathy.
Promoting Home and Community-Based Care
- Teaching Patients Self-Care
o the nurse teaches the patient and family about
the treatment plan, including the need to :
avoid all alcohol intake
adhere to a low-sodium diet
take medications as prescribed
check with the physician before taking any
new medications
skin care
the need to weigh the patient daily
to watch for and report signs and symptoms
of complications.
HEPATIC ENCEPHALOPATHY AND COMA
- is a life-threatening complication of liver disease that
occurs with profound liver failure.
- Patients with this condition have no overt signs of the
illness but do have abnormalities on
neuropsychologic testing
- Hepatic encephalopathy is the neuropsychiatric
manifestation of hepatic failure associated with
 portal hypertension and the shunting of blood from
the portal venous system into the systemic circulation

PATHOPHYSIOLOGY

- Two major alterations underlie its development in

acute and chronic liver disease.
- First hepatic insufficiency may result in
encephalopathy because of the inability of the liver to
detoxify toxic byproducts of metabolism.
- Second portal-systemic shunting, in which collateral
vessels develop as a result of portal hypertension,
allows elements of the portal blood to enter the - Inability to reproduce a simple figure
systemic circulation

Etiologic

- Amonia
o considered the major etiologic factor in the
development of encephalopathy.
o It enters the brain and excites peripheral
benzodiazepine type receptors on astrocyte cells,
thus increasing neurosteroid synthesis
o this then stimulates gamma-aminobutyric acid
(GABA) neurotransmission. GABA causes
depression of the central nervous system
o Ammonia inhibits neurotransmission and - fetor hepaticus
synaptic regulation o a sweet, slightly fecal odor to the breath that is
presumed to be of intestinal origin, may be
noticed.
o The odor has also been described as similar to
CLINICAL MANIFESTATIONS
that of freshly mowed grass, acetone, or old wine.
- minor mental changes and motor disturbances o Fetor hepaticus is prevalent with extensive
- The patient appears slightly confused collateral portal circulation in chronic liver
- unkempt disease.
- alterations in mood
- Alterations on sleep patterns.
o The patient tends to sleep during the day and has ASSESSMENT AND DIAGNOSTIC FINDINGS
restlessness and insomnia at night.
- As hepatic encephalopathy progresses: - electroencephalogram (EEG) shows:
o the patient may become difficult to awaken o generalized slowing, an increase in the amplitude
o completely disoriented with respect to time and of brain waves, and characteristic triphasic
place waves.
o With further progression, the patient lapses into o Patients should be referred for liver
frank coma and may have seizures. transplantation after this initial episode
- Asterixis (flapping tremor of the hands) may be seen
in stage II encephalopathy constructional apraxia
MEDICAL MANAGEMENT

- Focuses on identify and eliminating the precipitating

cause if possible:
 o initiating ammonia-lowering therapy
o minimizing potential medical complications of
cirrhosis and depressed consciousness
o reversing the underlying liver disease, if possible.
o Correction of the possible reasons for the
deterioration such as :
bleeding
electrolyte abnormalities
sedation, or azotemia is essential
- Lactulose (Cephulac) is administered to reduce serum
ammonia levels.
o side effects of lactulose include:
Intestinal bloating and cramps, which
usually disappear within a week.
To mask the sweet taste, which some
patients dislike, it can be diluted with fruit VIRAL HEPATITIS
juice.
- Viral hepatitis is a systemic, viral infection in which
necrosis and inflammation of liver cells produce a
NURSING MANAGEMENT characteristic cluster of clinical, biochemical, and
cellular changes.
- The nurse is responsible for maintaining a safe
environment to prevent injury, bleeding, and infection. Five types:
- The nurse administers the prescribed treatments and - hepatitis A, B, C, D, and E.
monitors the patient for the numerous potential - Hepatitis A and E are similar in mode of transmission
complications: (fecaloral route)
- pneumonia, and other respiratory complications. - whereas hepatitis B, C, and D share many other
- The nurse communicates with the patients Family to characteristics.
in- form them about the patients status and supports
them by explaining the procedures and treatments
that are part of the patients care. HEPATITIS A VIRUS

- formerly called infectious hepatitis, is caused by an

OTHER MANIFESTATIONS OF HEPATIC DYSFUNCTION: RNA virus of the Enterovirus family.

- Edema and bleeding MOT

- Vitamin deficiency - This form of hepatitis is transmitted primarily through
- Metabolic abnormalities the fecaloral route
- Puritus and other skin changes - by the ingestion of food or liquids infected by the
virus. It is more prevalent in countries with
overcrowding and poor sanitation

INCUBATION PERIOD

- incubation period is estimated to be between 2 to 6

weeks, with a mean of approximately 4 weeks
- The illness may be prolonged, lasting 4 to 8 weeks. It
usually lasts longer and is more severe in those older
than 40 years of age
 Because the patient often has an aversion to
food, gentle persistence and creativity may
CLINICAL MANIFESTATION
be required to stimulate appetite.
- Many patients are anicteric (without jaundice) and
symptomless.
- When symptoms appear, they resemble those of a NURSING MANAGEMENT
mild, flulike upper respiratory tract infection, with low-
- the nurse assists the patient and family in coping with
grade fever.
the temporary disability and fatigue that are common
- Anorexia, an early symptom, is often severe.
in hepatitis and instructs them to seek additional
- Later, jaundice and dark urine may become apparent.
health care if the symptoms persist or worsen
- Indigestion is present in varying degrees, marked by
- The nurse the specific guideline like what should be
vague epigastric distress, nausea, heartburn, and
avoid and importance of good sanitation
flatulence.
- Specific education for patient and family
- The patient may also develop a strong aversion to the
taste of cigarettes or the presence of cigarette smoke
and other strong odors.
HEPATITIS B VIRUS
ASSESSMENT AND DIAGNOSTIC FINDINGS
- the hepatitis B virus (HBV) is transmitted primarily
- Hepatitis A antigen may be found in the stool 7 to 10 through blood
days before illness and for 2 to 3 weeks after - percutaneous
symptoms appear - permucosal routes
- HAV antibodies are detectable in the serum, but - HBV can be found in :
usually not until symptoms appear. - Blood
- Analysis of subclasses of immunoglobulins can help - Saliva
determine whether the antibody represents acute or - semen,
past infection. - vaginal secretions
- can be transmitted through mucous membranes and
PREVENTION
breaks in the skin.
- Patients and their families are encouraged to follow - HBV is also transferred from carrier mothers to their
general precautions that can prevent transmission of infants
the virus o The infection usually is not transmitted via the
- Scrupulous handwashing umbilical vein but from the mother at the time of
- safe water supplies birth and during close contact afterward.
- proper control of sewage disposal are just a few of - The immune system is altered in the aged. A less
these prevention strategies. responsive immune system may be responsible for the
- It is recommended that the two-dose vaccine be given increased incidence and severity of hepatitis B
to adults 18 years of age or older, with the second
CLINICAL MANIFESTATION
dose given 6 to 12 months after the first.
- Fever and respiratory symptoms are rare;
MEDICAL MANAGEMENT
- some patients have :
- Bed rest during the acute stage and a diet that is both - arthralgias
acceptable to the patient and nutritious are part of - rashes.
the treatment and nursing care. - loss of appetite
o During the period of anorexia, the patient should - dyspepsia
receive: - abdominal pain
o frequent small feedings - generalized aching
o supplemented if necessary by IV fluids with - malaise
glucose. - weakness.
- Jaundice may or may not be evident.
- If jaundice occurs:
- light-colored stools
- dark urine accompany it.
- The liver may be tender and enlarged to
12 to 14 cm vertically.
The spleen is enlarged and palpable
ASSESSMENT AND DIAGNOSTIC
FINDINGS
HBcAghepatitis B core antigen (antigenic
material in an inner core)
HBsAghepatitis B surface antigen
(antigenic mate- rial on the viral surface, a
marker of active replication and infection)
HBeAgan independent protein
circulating in the blood
HBxAggene product of X gene of HBV
DNA
anti-HBcantibody to core antigen of
HBV; persists during the acute phase of
illness; may indicate con- tinuing HBV in the
liver
anti-HBsantibody to surface
determinants on HBV; detected during late
convalescence; usually indicates recovery
and development of immunity
anti-HBeantibody to hepatitis B eantigen;
usually signifies reduced infectivity
anti-HBxAgantibody to the hepatitis B
x-antigen; may indicate ongoing replication
of HBV
Prevention
Preventing transmissions
The use of disposable syringes,needles,
lancet
Good personal hygiene
Wear gloves
Laboratory guidelines should follow
Patient education regarding the disease
MEDICAL MANAGEMENT
The goals of treatment are to minimize
infectivity and liver inflammation and
decrease symptoms.
Bed rest
Adequate nutrition maintained
Two antiviral agents, lamivudine (Epivir) and
adefovir (Hepsera), oral nucleoside analogs
Proteins restricted
Measures to control the dyspeptic
symptoms and general malaise include the
use of antacids and antiemetics
but all medications should be avoided if
vomiting occurs.
If vomiting persists, the patient may require
hospitalization and fluid therapy.
Because of the mode of transmission, the
patient is evaluated for other bloodborne
diseases (eg, HIV infection
NURSING MANAGEMENT
The nurse identifies psychosocial issues and
concerns, particularly the effects of
separation from family and friends if the
patient is hospitalized during the acute and
infective stages.
Even if not hospitalized, the patient will be
unable to work and must avoid sexual
contact. surface antigen for its replication, only

Planning is required to minimize social people with hepatitis B are at risk for

isolation. hepatitis D. Anti-delta antibodies in the

Planning that includes the family helps to presence of HBAg on testing confirm the

reduce their fears and anxieties about the diagnosis.

spread of the disease. Most common in :

The nurse should emphasize no sexual IV or injection drug users

intercourse, strategies to prevent exchange hemodialysis patients

body fluids is recomended recipients of multiple blood

The nurse empasize follow up check up transfusions

HEPATITIS C Sexual contact with those with hepatitis

Blood transfusions and sexual contact are B

accounted in hepatitis c The symptoms of hepatitis D are

Parenteral means similar to those of hepatitis B, except

sharing of contaminated needles by IV that patients are more likely to develop

injection drug users and unintentional fulminant hepatitis and to progress to

needlesticks chronic active hepatitis and cirrhosis.

other injuries in health care workers Treatment is similar to that of other

People who are at risk forms of hepatitis

IV or injection drug users HEPATITIS E VIRUS

sexually active people with multiple hepatitis E virus (HEV) is transmitted by the

partners fecaloral route

patients receiving frequent transfusions principally through contaminated water in

those who require large volumes of blood areas with poor sanitation.

health care personnel The incubation period: 15 and 65 days.

The clinical course of hepa C is similar to hepatitis E resembles hepatitis A.

hepa B It has a self-limited course with an abrupt

Incubation period: 15 to 160 days onset

HEPATITIS D VIRUS Juandice is almost always present

Hepatitis D virus (delta agent) infection Prevention

occurs in some cases of hepatitis B. virus through good hygiene

Because the virus requires hepatitis B including handwashing

Hepatitis G virus and GB virus C Anorexia

It has long been believed that there is nausea

another non-AE agent causing hepatitis in vomiting

humans. Symptoms are more intense for more severly

The incubation period for posttransfusion toxic patients

hepatitis is 14 to 145 days DRUG-INDUCED HEPATITIS

People who recieved blood transfusion most common cause of acute liver failure

develop this disease Manifestations of sensitivity to a medication

Autoantibodies are absent may occur on the first day of its use or not

Clinical significance remains uncertain until several months later.

NONVIRAL HEPATITIS Sign and symptom

Drug-induced hepatitis is similar to acute Usually, the onset is abrupt

viral hepatitis, but parenchymal destruction with chills

tends to be more extensive fever

Medications that can lead to hepatitis rash

isoniazid (Nydrazid) pruritus

halothane (Fluothane) arthralgia

acetaminophen anorexia

methyldopa (Aldomet) nausea

certain antibiotics Later, there may be jaundice

antimetabolites dark urine

anesthetic agents. enlarged and tender liver.

TOXIC HEPATITIS After the offending medication is withdrawn,

toxic hepatitis resembles viral hepatitis. symptoms may gradually subside.

Obtaining a history of exposure to: ANATOMIC AND PHYSIOLOGIC

hepatotoxic chemicals OVERVIEW

medications THE GALLBLADDER

botanical agents pear-shaped, hollow, saclike organ.

other toxic agents assists in early 7.5 to 10 cm (3 to 4 in) long

treatment and removal of the causative lies in a shallow depression on the inferior

agent surface of the liver

Sign and symptom it is attached by loose connective tissue.

 The capacity of the gallbladder is 30 to 50 along with significant amounts of lecithin,

mL of bile. fatty acids, cholesterol, bilirubin, and bile

Its wall is composed largely of smooth salts.

muscle. The bile salts, together with cholesterol,

The gallbladder is connected to the common assist in emulsification of fats in the distal

bile duct by the cystic duct ileum.

gallbladder functions as a storage depot for They are then reabsorbed into the portal

bile. blood for return to the liver, after which they

Between meals, when the sphincter of Oddi are once again excreted into the bile

is closed, bile produced by the hepatocytes Approximately half of the bilirubin, a pigment

enters the gallbladder derived from the breakdown of red blood

During storage, a large portion of the water cells, is a component of bile

in bile is absorbed through the walls of the If the flow of bile is impeded (eg, by

gallbladder gallstones in the bile ducts), bilirubin does not

gallbladder is five to 10 times more enter the intestine

concentrated than that originally secreted by This causes increased renal excretion of

the liver urobilinogen, which results from conversion

When food enters the duodenum, the of bilirubin in the small intestine, and

gallbladder contracts and the sphincter of decreased excretion in the stool.

Oddi (located at the junction of the common These changes produce many of the signs

bile duct with the duodenum) relaxes. and symptoms seen in gallbladder disorders.

Relaxation of this sphincter allows the bile to

enter the intestine. ASSESSMENT

This response is mediated by secretion of HEALTH HISTORY

the hormone cholecystokinin-pancreozymin If liver function test is abnormal the patient

(CCK-PZ) from the intestinal wall is evaluated for liver disease.

Bile is composed of water and electrolytes: Health history focuses on:

sodium Exposure of the client to hepatoxic

potassium substances or infectious agents

calcium Patients occupation, recreational, and

chloride travel history

bicarbonate Travel history may assist the patients

exposure to hepatoxins melena

The patients history of alcohol and drug hematochezia (passage of bloody

use stools)

Lifestyles behaviors that increase the risk easy bruising

for exposure to infectious agents are changes in mental acuity

identified. personality changes

Evaluation of the patients past medical sleep disturbances

history to identify the risk factor for the decreased libido in men

development of liver disease secondary amenorrhea in women.

Current and past medical conditions PHYSICAL ASSESSMENT

Physiological or psychiatric nature The nurse assesses the patient for physical

Family history signs that may occur with liver dysfunction:

Question about familial liver: including the pallor often seen with

Origin of alcohol abuse chronic illness and jaundice.

Gallstone disease The skin, mucosa, and sclerae are

Genetic disease ( hematochromatosis, inspected for jaundice, and the

wilsons disease, antitrypsin disease ) extremities are assessed for muscle

Symptoms that may have their origin in liver atrophy, edema, and skin excoriation

disease but not specific to hepatic secondary to scratching.

dysfunction include : The nurse observes the skin for petechiae or

jaundice ecchymotic areas (bruises), spider angiomas,

malaise and palmar erythema.

weakness The male patient is assessed for unilateral or

fatigue bilateral gynecomastia and testicular atrophy

pruritus due to hormonal changes.

abdominal pain The patients cognitive status (recall,

fever memory, abstract thinking) and neurologic

anorexia status are assessed.

weight gain The nurse observes for:

edema general tremor

increasing abdominal girth asterixis

hematemesis weakness
 slurred speech. smooth.

The nurse assesses for the presence : The liver of a patient with cirrhosis is:

of an abdominal fluid wave (discussed small and hard

later). the liver of a patient with acute hepatitis:

The abdomen is palpated to assess liver soft

size and to detect any tenderness over the hand easily moves the edge.

the liver. The liver of a patient with viral hepatitis is:

The liver may be palpable in the right tender

upper quadrant. The liver of the patient that is alcoholic is

A palpable liver presents as a firm, sharp not tender

ridge with a smooth surface DIAGNOSTIC EVALUATION

The nurse estimates the size of the liver by: LIVER FUNCTION TEST

percussing its upper and lower borders. More than 70% of the parenchyma of the

If the liver is not palpable but tenderness liver may be damaged before liver function

is suspected, tapping the lower right test results become abnormal.

thorax briskly may elicit tenderness. Function is generally measured in terms of:

For comparison, the nurse then performs serum enzyme activity (ie, serum

a similar maneuver on the left lower aminotransferases, alkaline phosphatase,

thorax lactic dehydrogenase)

If the liver is palpable, the examiner notes serum concentrations of proteins

and records : (albumin and globulins), bilirubin,

its size ammonia, clotting factors, and lipids.

its consistency These test may be helpful in assessing

any tenderness patients with liver disease.

whether its outline is regular or irregular the nature and extent of hepatic dysfunction

If the liver is enlarged the degree to which it cannot be determined by these tests alone,

descends below the right costal margin is because other disorders can affect test

recorded to provide some indication of its results.

size. Serum aminotransferases (previously called

The examiner determines whether the livers: transaminases)

edge is sharp and smooth or blunt are sensitive indicators of injury to the

whether the enlarged liver is nodular or liver cells and are useful in detecting
acute liver disease such as hepatitis. REMEDY

Alanine aminotransferase (ALT), coagulation studies are obtained,

aspartate amino- transferase (AST), their values are noted

gamma-glutamyl transferase (GGT) (also abnormal results are treated before liver

called G-glutamyl transpeptidase) biopsy is performed.

are the most frequently used tests of Other techniques for liver biopsy are

liver damage. preferred if ascites or coagulation

ALT levels increase primarily in liver abnormalities exist.

disorders and may be used to monitor OTHER DIAGNOSTIC TEST

the course of hepatitis or cirrhosis or the Ultrasonography

effects of treatments that may be toxic computed tomography (CT)

to the liver. magnetic resonance imaging (MRI) are used

LIVER BIOPSY to identify normal structures and

Liver biopsy is the removal of a small amount abnormalities of the liver and biliary tree.

of liver tissue, usually through needle radioisotope liver scan

aspiration to assess liver size and hepatic blood flow

It permits examination of liver cells. and obstruction.

The most common indication is to evaluate Laparoscopy

diffuse disorders of the parenchyma and to insertion of a fiberoptic endoscope through

diagnose space-occupying lesions. a small abdominal incision

Liver biopsy is especially useful when clinical used to examine the liver and other pelvic

findings and laboratory tests are not structures.

diagnostic. It is also used to perform guided liver

liver biopsy can be performed percutaneously biopsy

with ultrasound guidance to determine the cause of ascites

transvenously through the right internal to diagnose and stage tumors of the liver

jugular vein to right hepatic vein under and other abdominal organs.

fluoroscopic control. MANIFESTATIONS OF HEPATIC

Liver biopsy can also be performed DYSFUNCTION

laparoscopically. Hepatic dysfunction results from damage to:

MAJOR COMPLICATION the livers parenchymal cells

Bleeding and bile peritonitis after liver biopsy directly from primary liver diseases
 indirectly from either obstruction of bile consequences of liver disease are numerous

flow and varied.

derangements of hepatic circulation Their ultimate effects are often

Liver dysfunction may be incapacitating or life-threatening

acute their presence is ominous

chronic Treatment often is difficult.

the latter is far more common JAUNDICE

Chronic liver disease When the bilirubin concentration in the blood

Disease processes that lead to is abnormally elevated

hepatocellular dysfunction may be caused all the body tissues, including the sclerae and

by infectious agents such as : the skin, become tinged yellow or greenish

bacteria yellow

viruses Jaundice becomes clinically evident when:

anoxia the serum bilirubin level exceeds 2.5

metabolic disorders mg/dL (43 fmol/L).

toxins Increased serum bilirubin levels and jaundice

medications may result from:

nutritional deficiencies impairment of hepatic uptake

hypersensitivity states. conjugation of bilirubin

most common cause of parenchymal damage excretion of bilirubin into the biliary

is malnutrition, especially that related to system.

alcoholism. several types of jaundice:

most common and significant manifestations hemolytic

of liver disease are : hepatocellular

jaundice obstructive jaundice

portal hypertension jaundice due to hereditary

ascites hyperbilirubinemia.

varices two types commonly associated with liver disease.

nutritional deficiencies (resulting from the Hepatocellular jaundice

inability of damaged liver cells to obstructive jaundice

metabolize certain vitamins) HEMOLYTIC JAUNDICE

hepatic encephalopathy or coma. is the result of an increased destruction of

the red blood cells, the effect of which is to carbon tetrachloride

flood the plasma with bilirubin so rapidly that chloroform

the liver phosphorus

although functioning normally, cannot arsenicals

excrete the bilirubin as quickly as it is certain medications

formed. alcohol.

encountered in patients with hemolytic Cirrhosis of the liver is a form of

transfusion reactions and other hemolytic hepatocellular disease that may produce

disorders. jaundice. It is usually associated with

the bilirubin in the blood is predominantly excessive alcohol intake

unconjugated or free. a late result of liver cell necrosis caused by

Fecal and urine urobilinogen levels are viral infection

increased, but the urine is free of bilirubin. In prolonged obstructive jaundice, cell

do not experience symptoms or damage eventually develops, so that both

complications as a result of the jaundice per types of jaundice (ie, obstructive and

se. hepatocellular jaundice) appear together

However, prolonged jaundice, even if mild, SIGN AND SYMPTOMS

predisposes to the formation of pigment may be mildly or severely ill

stones in the gallbladder, and extremely with lack of appetite

severe jaundice (levels of free bilirubin nausea

exceeding 20 to 25 mg/dL) poses a risk malaise

for brainstem damage. fatigue

HEPATOCELLULAR JAUNDICE weakness

caused by the inability of damaged liver cells possible weight loss.

to clear normal amounts of bilirubin from the In some cases of hepatocellular disease,

blood. jaundice may not be obvious

The cellular damage may be caused by: FOR CELLULAR NECROSIS

hepatitis viruses The serum bilirubin concentration and the

other viruses that affect the liver urine urobilinogen level may be elevated.

yellow fever virus In addition, AST and ALT levels may be

Epstein-Barr virus increased

medications or chemical toxins patient may report :

 headache tricyclic antidepressant agents

chills nitrofurantoin

fever if the cause is infectious androgens and estrogens

Depending on the cause and extent of the propylthiouracil

liver cell damage amoxicillin-clavulanic acid

hepatocellular jaundice may be completely erythromycin estolate.

reversible. bile cannot flow normally into the intestine

OBSTRUCTIVE JAUNDICE and becomes backed up into the liver

resulting from extrahepatic obstruction may substance.

be caused by : It is then reabsorbed into the blood and

occlusion of the bile duct from a carried throughout the entire body

gallstone staining the skin, mucous membranes, and

an inflammatory process sclerae.

a tumor It is excreted in the urine, which becomes

pressure from an enlarged organ (eg, deep orange and foamy.

liver, gallbladder). Because of the decreased amount of bile in

The obstruction may also involve the small the intestinal tract

bile ducts within the liver (ie, intra- hepatic the stools become light or clay colored.

obstruction); The skin may itch intensely, requiring

this may be caused by pressure on these repeated soothing baths.

channels from inflammatory swelling of the Dyspepsia and intolerance to fatty foods

liver or by an inflammatory exudate within may develop because of impaired fat

the ducts themselves. digestion in the absence of intestinal bile.

Intrahepatic obstruction resulting from stasis HERERIDATARY HYPERBILIRUBINEMIA

and inspissation (thickening) of bile within Increased serum bilirubin levels

the canaliculi may occur after the ingestion (hyperbilirubinemia), resulting from any of

of certain medications, which are referred to several inherited disorders

as cholestatic agents. Gilberts syndrome

Cholestatic agents is a familial disorder characterized by an

phenothiazine increased level of unconjugated bilirubin

antithyroid medications serum bilirubin levels are increased

sulfonylureas liver histology and liver function test results

are normal CLINICAL MANIFESTATION

there is no hemolysis. Increase abdominal girth

This syndrome affects 3% to 8% of the Rapid weight gain

population, predominantly males Short of breath

OTHER CONDITIONS CAUSED BY Uncomfortable from enlarged abdomen

INBORN ERRORS of BILARY Striae

METABOLISM: Distended veins may be visble over

Dubin-Johnson syndrome abdominal wall

chronic idiopathic jaundice, with pigment Umbilical hernias(patient with cirrhosis)

in the liver Fluid and electrolyte imbalnce

Rotors syndrome ASSESSMENT AND DIAGNOSTIC

chronic familial conjugated hyperbilirubinemia, FINDINGS

without pigment in the liver Percussion of the abdomen

the benign cholestatic jaundice of When fluid has accumulated in the peritoneal

pregnancy, with retention of conjugated cavity, the flanks bulge when the patient

bilirubin, probably secondary to unusual assumes a supine position.

sensitivity to the hormones of pregnancy; presence of fluid can be confirmed either by

benign recurrent intrahepatic cholestasis. percussing for shifting dullness or by

PORTAL HYPOTENSION detecting a fluid wave

the increased pressure throughout the portal A fluid wave is likely to be found only if a

venous system that results from obstruction large amount of fluid is present.

of blood flow through the damaged liver. Daily measurement and recording of

Commonly associated with hepatic cirhosis abdominal girth and body weight are

Also occur with non cirrhotic liver disease essential to assess the progression of

Although splenomegaly (enlarged spleen) with ascites and its response to treatment.

possible hypersplenism is a common MEDICAL MANAGEMENT

manifestation of portal hypertension Dietary modification

the two major consequences of portal Goal of treatment:

hypertension are : negative sodium balance to reduce fluid

ascites retention.

varices. AVOID:

ASCITES Table salts

 salty foods ascites and peripheral edema

salted butter 0.5 to 0.75 kg (1.1 to 1.65 lb) in patients

margarine without edema

all ordinary canned Fluid restriction is not attempted unless

frozen foods that are not specifically the serum sodium concentration is very

prepared for low-sodium (2-g sodium) diets low.

It takes 2 to 3 months for the patients taste POSSIBLE COMPLICATIONS

buds to adjust fluid and electrolyte disturbances

Commercial salt substitutes need to be hypovolemia

approved by the physician hypokalemia

because those that contain ammonia hyponatremia

could precipitate hepatic coma. hypochloremic alkalosis

Dietary control of ascites via strict sodium Encephalopathy

restriction is difficult to achieve at home. may be precipitated by dehydration

Non responders to this therapy may require and hypovolemia.

diuretics theraphy BED REST

Diuretics bed rest may be a useful therapy, especially

Spironolactone (Aldactone), an aldosterone for patients whose condition is refractory to

blocking agent, is most often the first-line diuretics.

therapy in patients with ascites from PARACENTESIS

cirrhosis. removal of fluid (ascites) from the peritoneal

Oral diuretics such as : cavity through a puncture or a small surgical

furosemide (Lasix) may be added but incision through the abdominal wall under

should be used cautiously, because longterm sterile conditions.

use may induce severe sodium Ultrasound guidance may be indicated in

depletion (hyponatremia). some patients who are at high risk for:

Ammonium chloride and acetazolamide bleeding because of an abnormal

(Diamox) are contraindicated because of coagulation profile

the possibility of precipitating hepatic those who have had previous abdominal

coma. surgery and may have adhesions.

Daily weight loss should not exceed was once considered a routine form of

1 to 2 kg (2.2 to 4.4 lb) in patients with treatment for ascites.

 Albumin infusions help to correct decreases to assess electrolyte balance, response

in effective arterial blood volume to therapy, and indicators of

that lead to sodium retention. encephalopathy.

TRANSJUGULAR INTRAHEPATIC Promoting Home and Community-Based Care

PORTOSYSTEMIC SHUNT Teaching Patients Self-Care

Transjugular intrahepatic portosystemic the nurse teaches the patient and family

shunt (TIPS) is a method of treating ascites about the treatment plan, including the

in which a cannula is threaded into the portal need to :

vein by the transjugular route avoid all alcohol intake

To reduce portal hypertension adhere to a low-sodium diet

expandable stent is inserted to serve as an take medications as prescribed

intrahepatic shunt between the portal check with the physician before

circulation and the hepatic vein. taking any new medications

TIPS is the treatment of choice for skin care

refractive ascites. the need to weigh the patient daily

It is extremely effective in decreasing sodium to watch for and report signs and

retention, improving the renal response to symptoms of complications.

diuretic therapy, and preventing recurrence HEPATIC ENCEPHALOPATHY AND

of fluid accumulation. COMA

OTHER METHODS OF TREATMENT is a life-threatening complication of liver

For patients who are not candidates for liver disease that occurs with profound liver

transplant because of: failure.

High complication Patients with this condition have no overt

High incidence of shunt failure signs of the illness but do have abnormalities

NURSING MANAGEMENT on neuropsychologic testing

nursing measures include assessment and Hepatic encephalopathy is the

documentation of : neuropsychiatric manifestation of hepatic

intake and output failure associated with portal hypertension

abdominal girth and the shunting of blood from the portal

daily weight to assess fluid status. venous system into the systemic circulation

The nurse monitors serum ammonia and PATHOPHYSIOLOGY

electrolyte levels Two major alterations underlie its

development in acute and chronic liver and has restlessness and insomnia at

disease. night.

First hepatic insufficiency may result in As hepatic encephalopathy progresses:

encephalopathy because of the inability of the patient may become difficult to awaken

the liver to detoxify toxic byproducts of completely disoriented with respect to time

metabolism. and place

Second portal-systemic shunting, in which With further progression, the patient lapses

collateral vessels develop as a result of portal into frank coma and may have seizures.

hypertension, allows elements of the portal Asterixis (flapping tremor of the hands) may

blood to enter the systemic circulation be seen in stage II encephalopathy

Etiologic constructional apraxia

Amonia Inability to reproduce a simple figure

considered the major etiologic factor in fetor hepaticus

the development of encephalopathy. a sweet, slightly fecal odor to the breath

It enters the brain and excites peripheral that is presumed to be of intestinal

benzodiazepine type receptors on origin, may be noticed.

astrocyte cells, thus increasing The odor has also been described as

neurosteroid synthesis similar to that of freshly mowed grass,

this then stimulates gamma-aminobutyric acetone, or old wine.

acid (GABA) neurotransmission. GABA Fetor hepaticus is prevalent with

causes depression of the central nervous extensive collateral portal circulation in

system chronic liver disease.

Ammonia inhibits neurotransmission and ASSESSMENT AND DIAGNOSTIC

synaptic regulation FINDINGS

CLINICAL MANIFESTATIONS electroencephalogram (EEG) shows:

minor mental changes and motor generalized slowing, an increase in the

disturbances amplitude of brain waves, and

The patient appears slightly confused characteristic triphasic waves.

unkempt Patients should be referred for liver

alterations in mood transplantation after this initial episode

Alterations on sleep patterns. MEDICAL MANAGEMENT

The patient tends to sleep during the day Focuses on identify and eliminating the
precipitating cause if possible: procedures and treatments that are part of

initiating ammonia-lowering therapy the patients care.

minimizing potential medical OTHER MANIFESTATIONS OF HEPATIC

complications of cirrhosis and depressed DYSFUNCTION:

consciousness Edema and bleeding

reversing the underlying liver disease, if Vitamin deficiency

possible. Metabolic abnormalities

Correction of the possible reasons for Puritus and other skin changes

the deterioration such as : VIRAL HEPATITIS

bleeding Viral hepatitis is a systemic, viral infection in

electrolyte abnormalities which necrosis and inflammation of liver cells

sedation, or azotemia is essential produce a characteristic cluster of clinical,

Lactulose (Cephulac) is administered to biochemical, and cellular changes.

reduce serum ammonia levels. Five types:

side effects of lactulose include: hepatitis A, B, C, D, and E.

intestinal bloating and cramps, which Hepatitis A and E are similar in mode of

usually disappear within a week. transmission (fecaloral route)

To mask the sweet taste, which some whereas hepatitis B, C, and D share many

patients dislike, it can be diluted with other characteristics.

fruit juice. HEPATITIS A VIRUS

NURSING MANAGEMENT formerly called infectious hepatitis, is caused

The nurse is responsible for maintaining a by an RNA virus of the Enterovirus family.

safe environment to prevent injury, bleeding, MOT

and infection. This form of hepatitis is transmitted primarily

The nurse administers the prescribed through the fecaloral route

treatments and monitors the patient for the by the ingestion of food or liquids infected by

numerous potential complications: the virus. It is more prevalent in countries

pneumonia, and other respiratory with overcrowding and poor sanitation

complications. INCUBATION PERIOD

The nurse communicates with the patients incubation period is estimated to be between

Family to in- form them about the patients 2 to 6 weeks, with a mean of approximately

status and supports them by explaining the 4 weeks

 The illness may be prolonged, lasting 4 to 8 prevent transmission of the virus

weeks. It usually lasts longer and is more Scrupulous handwashing

severe in those older than 40 years of age safe water supplies

CLINICAL MANIFESTATION proper control of sewage disposal are

Many patients are anicteric (without just a few of these prevention strategies.

jaundice) and symptomless. It is recommended that the two-dose

When symptoms appear, they resemble vaccine be given to adults 18 years of age

those of a mild, flulike upper respiratory or older, with the second dose given 6 to 12

tract infection, with low- grade fever. months after the first.

Anorexia, an early symptom, is often severe. MEDICAL MANAGEMENT

Later, jaundice and dark urine may become Bed rest during the acute stage and a diet

apparent. that is both acceptable to the patient and

Indigestion is present in varying degrees, nutritious are part of the treatment and

marked by vague epigastric distress, nausea, nursing care.

heartburn, and flatulence. During the period of anorexia, the patient

The patient may also develop a strong should receive:

aversion to the taste of cigarettes or the frequent small feedings

presence of cigarette smoke and other supplemented if necessary by IV fluids

strong odors. with glucose.

ASSESSMENT AND DIAGNOSTIC Because the patient often has an

FINDINGS aversion to food, gentle persistence

Hepatitis A antigen may be found in the and creativity may be required to

stool 7 to 10 days before illness and for 2 to stimulate appetite.

3 weeks after symptoms appear NURSING MANAGEMENT

HAV antibodies are detectable in the serum, the nurse assists the patient and family in

but usually not until symptoms appear. coping with the temporary disability and

Analysis of subclasses of immunoglobulins fatigue that are common in hepatitis and

can help determine whether the antibody instructs them to seek additional health care

represents acute or past infection. if the symptoms persist or worsen

PREVENTION The nurse the specific guideline like what

Patients and their families are encouraged should be avoid and importance of good

to follow general precautions that can sanitation

 Specific education for patient and family malaise

HEPATITIS B VIRUS weakness.

the hepatitis B virus (HBV) is transmitted Jaundice may or may not be evident.

primarily through blood If jaundice occurs:

percutaneous light-colored stools

permucosal routes dark urine accompany it.

HBV can be found in : The liver may be tender and enlarged to

blood 12 to 14 cm vertically.

saliva The spleen is enlarged and palpable

semen, ASSESSMENT AND DIAGNOSTIC

vaginal secretions FINDINGS

can be transmitted through mucous HBcAghepatitis B core antigen (antigenic

membranes and breaks in the skin. material in an inner core)

HBV is also transferred from carrier HBsAghepatitis B surface antigen

mothers to their infants (antigenic mate- rial on the viral surface, a

The infection usually is not transmitted marker of active replication and infection)

via the umbilical vein but from the HBeAgan independent protein

mother at the time of birth and during circulating in the blood

close contact afterward. HBxAggene product of X gene of HBV

The immune system is altered in the aged. A DNA

less responsive immune system may be anti-HBcantibody to core antigen of

responsible for the increased incidence and HBV; persists during the acute phase of

severity of hepatitis B illness; may indicate con- tinuing HBV in the

CLINICAL MANIFESTATION liver

Fever and respiratory symptoms are rare; anti-HBsantibody to surface

some patients have : determinants on HBV; detected during late

arthralgias convalescence; usually indicates recovery

rashes. and development of immunity

loss of appetite anti-HBeantibody to hepatitis B eantigen;

dyspepsia usually signifies reduced infectivity

abdominal pain anti-HBxAgantibody to the hepatitis B

generalized aching x-antigen; may indicate ongoing replication

of HBV patient is hospitalized during the acute and

Prevention infective stages.

Preventing transmissions Even if not hospitalized, the patient will be

The use of disposable syringes,needles, unable to work and must avoid sexual

lancet contact.

Good personal hygiene Planning is required to minimize social

Wear gloves isolation.

Laboratory guidelines should follow Planning that includes the family helps to

Patient education regarding the disease reduce their fears and anxieties about the

MEDICAL MANAGEMENT spread of the disease.

The goals of treatment are to minimize The nurse should emphasize no sexual

infectivity and liver inflammation and intercourse, strategies to prevent exchange

decrease symptoms. body fluids is recomended

Bed rest The nurse empasize follow up check up

Adequate nutrition maintained HEPATITIS C

Two antiviral agents, lamivudine (Epivir) and Blood transfusions and sexual contact are

adefovir (Hepsera), oral nucleoside analogs accounted in hepatitis c

Proteins restricted Parenteral means

Measures to control the dyspeptic sharing of contaminated needles by IV

symptoms and general malaise include the injection drug users and unintentional

use of antacids and antiemetics needlesticks

but all medications should be avoided if other injuries in health care workers

vomiting occurs. People who are at risk

If vomiting persists, the patient may require IV or injection drug users

hospitalization and fluid therapy. sexually active people with multiple

Because of the mode of transmission, the partners

patient is evaluated for other bloodborne patients receiving frequent transfusions

diseases (eg, HIV infection those who require large volumes of blood

NURSING MANAGEMENT health care personnel

The nurse identifies psychosocial issues and The clinical course of hepa C is similar to

concerns, particularly the effects of hepa B

separation from family and friends if the Incubation period: 15 to 160 days
HEPATITIS D VIRUS Juandice is almost always present

Hepatitis D virus (delta agent) infection Prevention

occurs in some cases of hepatitis B. virus through good hygiene

Because the virus requires hepatitis B including handwashing

surface antigen for its replication, only Hepatitis G virus and GB virus C

people with hepatitis B are at risk for It has long been believed that there is

hepatitis D. Anti-delta antibodies in the another non-AE agent causing hepatitis in

presence of HBAg on testing confirm the humans.

diagnosis. The incubation period for posttransfusion

Most common in : hepatitis is 14 to 145 days

IV or injection drug users People who recieved blood transfusion

hemodialysis patients develop this disease

recipients of multiple blood Autoantibodies are absent

transfusions Clinical significance remains uncertain

Sexual contact with those with hepatitis NONVIRAL HEPATITIS

B Drug-induced hepatitis is similar to acute

The symptoms of hepatitis D are viral hepatitis, but parenchymal destruction

similar to those of hepatitis B, except tends to be more extensive

that patients are more likely to develop Medications that can lead to hepatitis

fulminant hepatitis and to progress to isoniazid (Nydrazid)

chronic active hepatitis and cirrhosis. halothane (Fluothane)

Treatment is similar to that of other acetaminophen

forms of hepatitis methyldopa (Aldomet)

HEPATITIS E VIRUS certain antibiotics

hepatitis E virus (HEV) is transmitted by the antimetabolites

fecaloral route anesthetic agents.

principally through contaminated water in TOXIC HEPATITIS

areas with poor sanitation. toxic hepatitis resembles viral hepatitis.

The incubation period: 15 and 65 days. Obtaining a history of exposure to:

hepatitis E resembles hepatitis A. hepatotoxic chemicals

It has a self-limited course with an abrupt medications

onset botanical agents

 other toxic agents assists in early 7.5 to 10 cm (3 to 4 in) long

treatment and removal of the causative lies in a shallow depression on the inferior

agent surface of the liver

Sign and symptom it is attached by loose connective tissue.

Anorexia The capacity of the gallbladder is 30 to 50

nausea mL of bile.

vomiting Its wall is composed largely of smooth

Symptoms are more intense for more severly muscle.

toxic patients The gallbladder is connected to the common

DRUG-INDUCED HEPATITIS bile duct by the cystic duct

most common cause of acute liver failure gallbladder functions as a storage depot for

Manifestations of sensitivity to a medication bile.

may occur on the first day of its use or not Between meals, when the sphincter of Oddi

until several months later. is closed, bile produced by the hepatocytes

Sign and symptom enters the gallbladder

Usually, the onset is abrupt During storage, a large portion of the water

with chills in bile is absorbed through the walls of the

fever gallbladder

rash gallbladder is five to 10 times more

pruritus concentrated than that originally secreted by

arthralgia the liver

anorexia When food enters the duodenum, the

nausea gallbladder contracts and the sphincter of

Later, there may be jaundice Oddi (located at the junction of the common

dark urine bile duct with the duodenum) relaxes.

enlarged and tender liver. Relaxation of this sphincter allows the bile to

After the offending medication is withdrawn, enter the intestine.

symptoms may gradually subside. This response is mediated by secretion of

ANATOMIC AND PHYSIOLOGIC the hormone cholecystokinin-pancreozymin

OVERVIEW (CCK-PZ) from the intestinal wall

THE GALLBLADDER Bile is composed of water and electrolytes:

pear-shaped, hollow, saclike organ. sodium

 potassium

calcium

chloride

bicarbonate

along with significant amounts of lecithin,

fatty acids, cholesterol, bilirubin, and bile

salts.

The bile salts, together with cholesterol,

assist in emulsification of fats in the distal

ileum.

They are then reabsorbed into the portal

blood for return to the liver, after which they

are once again excreted into the bile

Approximately half of the bilirubin, a pigment

derived from the breakdown of red blood

cells, is a component of bile

If the flow of bile is impeded (eg, by

gallstones in the bile ducts), bilirubin does not

enter the intestine

This causes increased renal excretion of

urobilinogen, which results from conversion

of bilirubin in the small intestine, and

decreased excretion in the stool.

These changes produce many of the signs

and symptoms seen in gallbladder disorders.