Hepatitis: - Defined As

HEPATITIS
• Defined as inflammation of the liver and characterized

by the presence of inflammatory cells in the tissue of
the organ.
• Causes of hepatitis: drugs, toxins, alcohol, viral
infections(A,B,C,D,E), physical damage and other
infections.
Prepared by :Fikiru Y(MSc)

HEPATITIS…
• Hepatocellular necrosis and inflammatory cell
infiltration of the liver are common pathologic features.
• There are two types of hepatitis, which are defined
based on duration:
I. Acute hepatitis: lasts for about 6 months or less.
II. Chronic hepatitis: sustained inflammatory response for
over 6 months.

HEPATITIS…
• A group of viruses known as the hepatitis viruses
cause most liver damages worldwide.
• Viral hepatitis is a systemic viral infection in

which necrosis and inflammation of liver cells
produce a characteristic cluster of clinical,
biochemical, and cellular changes.
HEPATITIS…
Five types of viral hepatitis:
– Hepatitis A
– Hepatitis B
– Hepatitis C
– Hepatitis D
– Hepatitis E.

Epidemiology
• Hepatitis is easily transmitted and causes high
morbidity and prolonged loss of time from school or
employment.
• Hepatitis A is responsible for 37% of all cases, and
hepatitis B is the offending agent in 18% of cases.

Epidemiology…
• In particular, types B and C lead to chronic disease in
hundreds of millions of people and, together, are the
most common cause of liver cirrhosis and cancer.
• Hepatitis A and E are similar in mode of transmission
(fecal–oral route).
• Hepatitis B, C, and D share many characteristics.

Hepatitis A Virus (HAV)
• Hepatitis A is an acute systemic infection caused by
the hepatitis A virus (HAV) that primarily affects the
liver.
• Hepatitis A, formerly called infectious hepatitis, is

caused by an RNA virus of the Enterovirus family.

Hepatitis A Virus (HAV)…
• This form of hepatitis is transmitted primarily through
the fecal–oral route, by the ingestion of food or liquids
infected by the virus.
• The virus is present in the faeces of infected persons
and is most often transmitted through consumption of
contaminated water or food.
• It is more prevalent in countries with overcrowding and
poor sanitation.
Hepatitis A Virus (HAV)…
• Most patients recover from hepatitis A; it rarely
progresses to acute liver necrosis or fulminant hepatitis
resulting in cirrhosis of the liver or death.
• The mortality rate of hepatitis A is approximately 1%
to 2% for older people.

Clinical Manifestations
• Constitutional symptoms 1–2 weeks preceding the

onset of jaundice includes:
 Anorexia, nausea, vomiting, fatigue,
malaise ,arthralgias,myalgias,headache,photophob
ia,pharyngitis,Cough,coryza (nasal
congestion),low-grade fever.

Clinical Manifestations…
• Later, jaundice and dark urine may become apparent.
• Indigestion is present in varying degrees, marked by

vague epigastric distress, nausea, heartburn, and
flatulence.
• Symptoms may be mild in children; in adults, they may

be more severe and the course of the disease prolonged.

Assessment and Diagnostic Findings
• The liver often moderately enlarged for a few days after
onset; other than jaundice, there are few other physical
signs.
• Serum alanine aminotransferase (ALT), Serum aspartate
aminotransferase (AST), Serum alkaline phosphatase
(ALP) level may be normal or only mildly elevated.

Assessment and Diagnostic Findings…
• HAV antibodies are detectable in the serum, but
usually not until symptoms appear.
• Detection of IgM anti-HAV during acute illness,
which disappears 3-6 months latter.
• Increased Serum bilirubin.

• Jaundice is usually visible in the sclera or skin when

the serum bilirubin value is > 43 μmol/L (2.5 mg/dL).
• Albumin level: Decrease (uncommon in
uncomplicated cases).

Prevention
• A number of strategies exist to prevent transmission
of HAV.
• Scrupulous hand washing, safe water supplies, and
proper control of sewage disposal are just a few of
these prevention strategies.
• Heat foods at temperatures >185°F (>85°C) for 1
minute
• Preexposure immunoprophylaxis (Vaccine)
• Post exposure immunoprophylaxis

Medical Management
• Supportive care like bed rest during the acute stage

and a diet that is both acceptable to the patient and
nutritious are part of the treatment and nursing care.
• During the period of anorexia, the patient should
receive frequent small feedings, supplemented if
necessary by IV fluids with glucose.

Medical Management…
• The patient’s sense of well-being and laboratory test
results are generally appropriate guides to bed rest and
restriction of physical activity.
• Avoidance of alcohol and drugs metabolized by the
liver.
• Avoidance of drugs capable of producing adverse
reactions, such as cholestasis.
Hepatitis B Virus
• HBV is a small, double-shelled virus in the family

Hepadnaviridae .
• HBV contains numerous antigenic components,
including HBsAg, hepatitis B core antigen (HBcAg),
and hepatitis B e antigen (HBeAg).
• Humans are the only known host for HBV.

Hepatitis B Virus…
• An estimated 2 billion persons worldwide have been

infected with HBV.
• HBV infection is an established cause of acute and
chronic hepatitis and cirrhosis.
• It is the cause of up to 50% of hepatocellular
carcinomas (HCC).

Hepatitis B Virus…
• HBsAg can be identified in serum 30 to 60 days after
exposure to HBV and persists for variable periods .
• Hepatitis B virus (HBV) is transmitted primarily
through blood (percutaneous and permucosal routes).
• HBV can be found in blood, saliva, semen, and
vaginal secretions and can be transmitted through
mucous membranes and breaks in the skin.

Risk Factors for Hepatitis B
 Frequent exposure to blood, blood products, or other body
fluids.
 Health care workers: hemodialysis staff,, personnel at risk for
needlesticks injury.
 Close contact with carrier of HBV.
 Travel to or residence in area with uncertain sanitary
conditions
 Multiple sexual partners.
• Clinically, the disease closely resembles hepatitis A, but

the incubation period is much longer (1 to 6 months).
• The patient may have loss of appetite, dyspepsia,
abdominal pain, generalized aching, malaise, and
weakness. Jaundice may or may not be evident..
• Fever and respiratory symptoms are rare; some patients
have arthralgias and rashes.
• HBsAg is the most commonly used test for diagnosing

acute HBV infections or detecting carriers.
• HBsAg can be detected as early as 1 or 2 weeks and as
late as 11 or 12 weeks after exposure to HBV when
sensitive assays are used.
• Patients with HBsAg that persists for 6 months or longer
after acute infection are considered to be HBsAg carriers
• HBeAg is the next antigen of HBV to appear in the

serum.
• It usually appears within 1 week of the appearance of
HBsAg but before changes in aminotransferase levels; it
disappears from the serum within 2 weeks.
• HBcAg is not always detected in the serum in HBV
infection.
• IgM anti-HBc appears in persons with acute disease

about the time of illness onset and indicates recent
infection with HBV.
• A negative test for IgM-anti-HBc together with a
positive test for HBsAg in a single blood sample
identifies a chronic HBV infection.

Prevention
Preventing Transmission:
• Screening of blood donors for the presence of
hepatitis B antigens further decreases the risk of
transmission by blood transfusion.
• The use of disposable syringes, needles, and lancets
have reduced the risk of spreading this infection from
one patient to another.
Prevention…
Active Immunization: Hepatitis B Vaccine:
• Active immunization is recommended for people who
are at high risk for hepatitis B (e.g., health care
personnel, hemodialysis patients).
• A yeast-recombinant hepatitis B vaccine (Recombivax
HB) is used to provide active immunity and has shown
rates of protection greater than 90% in healthy people.

Prevention…
• Hepatitis B vaccines are administered intramuscularly
in three doses; the second and third doses are given 1
and 6 months, respectively, after the first dose.
• The vaccine produces active immunity to HBV in 90%
of healthy people.
• Hepatitis B vaccination is recommended for all
unvaccinated people being evaluated for a sexually
transmitted disease (STD).
Prevention…
Passive Immunity: Hepatitis B Immune Globulin:
• Hepatitis B immune globulin (HBIG) provides
passive immunity to hepatitis B and is indicated for
people exposed to HBV who have never had hepatitis
B and have never received hepatitis B vaccine.

Medical Management
• The goals of treatment are to minimize infectivity and

liver inflammation and decrease symptoms.
• Of all the agents that have been used to treat chronic
type B viral hepatitis, alpha-interferon as the single
modality of therapy that offers the most promise.

• Interferon must be administered by injection and has

significant side effects, including fever, chills,
anorexia, nausea, myalgias, and fatigue.
• Two antiviral agents, lamivudine and adefovir, oral
nucleoside analogs, have been approved for use in
chronic hepatitis B in the United States.

• Adequate nutrition should be maintained.

• Proteins are restricted if symptoms indicate that the
liver’s ability to metabolize protein byproducts is
impaired.
• Bed rest may be recommended, regardless of other
treatment.

Hepatitis C Virus
• Hepatitis C can be developed by infection with the

hepatitis C virus, which at first was related to
intravenous drugs or blood transfusions.
• Blood transfusions and sexual contact once accounted
for most cases of hepatitis C in the United States.

Hepatitis C Virus…
• The hepatitis C virus is responsible for almost a half of

cases of cirrhosis that end in the loss of the patient' s
life and more than 70 percent of people suffering from
chronic hepatitis.
• HCV is the underlying cause of about one third of cases
of hepatocellular carcinoma, and it is the most common
reason for live transplantation
Hepatitis C Virus…
People who are at particular risk for hepatitis C include:
– sexually active people with multiple partners,
– patients receiving frequent transfusions, those who
require large volumes of blood, and
– health care personnel.
However, a chronic carrier state occurs frequently,

and there is an increased risk of chronic liver disease
including cirrhosis Prepared
or liver cancer, after hepatitis C.
by :Fikiru Y(MSc)
Diagnostic Tests
• HCV antibody - generally used to diagnose hepatitis
C infection.
• HCV-RNA - various techniques are available e.g.
PCR and branched DNA. May be used to diagnose
HCV infection in the acute phase. However, its main
use is in monitoring the response to antiviral therapy.

Medical management
• Alcohol and medications that may affect the liver
should be avoided.
• Studies have demonstrated that a combination of two
antiviral agents, interferon and ribavirin (Rebetol) is
effective in producing improvement in patients with
hepatitis C and in treating relapses.

Medical management…
• Screening of blood has reduced the incidence of

hepatitis C associated with blood transfusion, and
public health programs are helping to reduce the
number of cases associated with shared needles in IV
or injection drug use.

Hepatitis D Virus
• Hepatitis D virus (delta agent) infection occurs in

some cases of hepatitis B.
• Anti-delta antibodies in the presence of HBAg on
testing confirm the diagnosis.
• The incubation period varies between 30 and 150
days (Goldman & Ausiello, 2008).

Hepatitis D Virus…
• Hepatitis D is common among IV or injection drug
users, hemodialysis patients, and recipients of
multiple blood transfusions.
• Sexual contact with those with hepatitis B is
considered to be an important mode of transmission
of hepatitis B and D.

Hepatitis D Virus…
• Treatment is similar to that of other forms of
hepatitis; interferon as a specific treatment for
hepatitis D is under investigation.

Hepatitis E Virus
• It is believed that hepatitis E virus (HEV) is
transmitted by the fecal–oral route, principally through
contaminated water in areas with poor sanitation.
• The incubation period is variable, estimated to range
between 15 and 65 days.
• In general, hepatitis E resembles hepatitis A.

Hepatitis E Virus…
• It has a self-limited course with an abrupt onset.

• Jaundice is almost always present.
• Hepatitis E predominantly affects those aged 15 to 40
years of age.
• Chronic forms do not develop.

Hepatitis E Virus…
• Avoiding contact with the virus through good

hygiene, including hand washing, is the major
method of prevention of hepatitis E.
• The effectiveness of immune globulin in protecting
against hepatitis E virus is uncertain.

NONVIRAL HEPATITIS
• Certain chemicals have toxic effects on the liver and

produce acute liver cell necrosis or toxic hepatitis when
inhaled, injected parenterally, or are taken by mouth.
• The chemicals most commonly implicated in this
disease are carbon tetrachloride, phosphorus,
chloroform, and gold compounds.

NONVIRAL HEPATITIS…
• Drug-induced hepatitis is similar to acute viral

hepatitis, but parenchymal destruction tends to be more
extensive.
• Medications that can lead to hepatitis include isoniazid
(Nydrazid), halothane (Fluothane), acetaminophen,
methyldopa (Aldomet), and certain antibiotics,
antimetabolites, and anesthetic agents.
HEPATIC CIRRHOSIS
 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:
1. Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas.

HEPATIC CIRRHOSIS…
• This is most frequently caused by chronic alcoholism and
is the most common type of cirrhosis.
2. Post necrotic cirrhosis: Results from destruction of liver
cells secondary to infection, exposure to hepatotoxins or
chemicals
• In this type of cirrhosis, there are broad bands(wide
spread) of scar tissue.

HEPATIC CIRRHOSIS…
3. Biliary cirrhosis, in which scarring occurs in the liver

around the bile ducts.
• This type of cirrhosis usually results from chronic
biliary obstruction and infection (cholangitis); it is
much less common than the other two types.

Pathophysiology
• several factors have been implicated in the etiology of

cirrhosis, alcohol consumption is considered the
major causative factor.
• Although nutritional deficiency with reduced protein
intake contributes to liver destruction in cirrhosis.

Pathophysiology…
• Other factors may play a role, including exposure to
certain chemicals (carbon tetrachloride, chlorinated
naphthalene, arsenic, or phosphorus) or infection.
• Most patients are between 40 and 60 years of age.
• Each year more than 27,000 people die of chronic liver
diseases and cirrhosis in the United States.

Pathophysiology…
• Alcoholic cirrhosis is characterized by episodes of

necrosis involving the liver cells, which sometimes
occur repeatedly throughout the course of the disease.
• The destroyed liver cells are gradually replaced by scar
tissue.
• Eventually, the amount of scar tissue exceeds that of the
functioning liver tissue.
• Signs and symptoms of cirrhosis increase in severity as
the disease progresses.
• Their severity is used to categorize the disorder as
compensated or decompensated cirrhosis.
• The hallmarks of decompensated cirrhosis result from
failure of the liver to synthesize proteins, clotting factors,
and other substances and manifestations of portal
hypertension.
• Early in the course of cirrhosis, the liver tends to be

large, and the cells are loaded with fat.
• The liver is firm and has a sharp edge that is noticeable
on palpation.
• Later in the disease, the liver decreases in size as scar
tissue contracts the liver tissue.
• The liver edge, if palpable, is nodular.
• Portal obstruction and ascites, late manifestations of

cirrhosis, are caused partly by chronic failure of liver
function and partly by obstruction of the portal
circulation.
• Almost all of the blood from the digestive organs is
collected in the portal veins and carried to the liver.

• Because a cirrhotic liver does not allow free blood

passage, blood backs up into the spleen and the GI
tract, and these organs become congested and
therefore cannot function properly.
• Fluid rich in protein may accumulate in the peritoneal
cavity, producing ascites.

• Bacterial peritonitis may develop in patients with

cirrhosis and ascites in the absence of an intra-
abdominal source of infection or an abscess.
• This condition is referred to as spontaneous bacterial
peritonitis (SBP).
• Bacteremia due to translocation of intestinal flora is
believed to be the most likely route of infection.
• The obstruction to blood flow through the liver

caused by fibrotic changes also results in the
formation of collateral blood vessels in the GI system
and shunting of blood from the portal vessels into
blood vessels with lower pressures.

• As a result, the patient with cirrhosis often has

prominent, distended abdominal blood vessels, which
are visible on abdominal inspection (caput medusae)
and distended blood vessels throughout the GI tract.
• The esophagus, stomach, and lower rectum are
common sites of collateral blood vessels.

• Another late symptom of cirrhosis is edema due to

reduced plasma albumin concentration.
• Additional clinical manifestations include
deterioration of mental and cognitive function with
impending hepatic encephalopathy and hepatic coma

• Many diagnostic tests provide information about liver

function.
• In severe parenchymal liver dysfunction, the serum
albumin level tends to decrease.
• Enzyme tests indicate liver cell damage: serum alkaline
phosphatase, AST, ALT, and GGT levels increase.

• Bilirubin tests are performed to measure bile
excretion or retention; increased levels of bilirubin
can occur with cirrhosis and other liver disorders.
• Ultrasound scanning is used to measure the difference
in density of parenchymal cells and scar tissue.

• CT, MRI, and radioisotope liver scans give

information about liver size and hepatic blood flow
and obstruction.
• Diagnosis is confirmed by liver biopsy.

Medical Management
• The management of the patient with cirrhosis is usually
based on the presenting symptoms.
• Vitamins and nutritional supplements promote healing
of damaged liver cells and improve the patient’s general
nutritional status.
• Potassium-sparing diuretics such as spironolactone or
triamterene (Dyrenium) may be indicated to decrease
ascites. Prepared by :Fikiru Y(MSc)
• An adequate diet and avoidance of alcohol are
essential.
• Restrict protein intake in clients with advanced liver
disease, because it increase the ammonia in the
intestine, precipitating hepatic encephalopathy
• Primary biliary cirrhosis has been treated with
ursodeoxycholic acid (Actigall, URSO) to improve
liver function. Prepared by :Fikiru Y(MSc)
Nursing Management
• Nursing interventions are directed toward promoting

patient’s rest, improving nutritional status, providing
skin care, reducing risk of injury, and monitoring and
managing potential complications.
• The patient with cirrhosis requires rest, elimination of
alcohol and other supportive measures to permit the
liver to reestablish its functional ability.
Nursing Management…
• If the patient is hospitalized, weight and fluid intake

and output are measured and recorded daily.
• Rest reduces the demands on the liver and increases
the liver’s blood supply.
• The patient with cirrhosis without ascites, edema, or
signs of impending hepatic coma should receive a
nutritious, high-protein diet, if tolerated,
supplemented by vitamins of the B complex, as well
as A, C, and K.
• Providing careful skin care is important because of

subcutaneous edema, the patient’s immobility,
jaundice, and increased susceptibility to skin
breakdown and infection.
• Irritating soaps and the use of adhesive tape are
avoided to prevent trauma to the skin.

Portal Hypertension
• is the increased pressure throughout the portal

venous system that results from obstruction of blood
flow through the damaged liver.
• Commonly associated with hepatic cirrhosis.

Portal Hypertension…
• Although splenomegaly(enlarged spleen) with

possible hypersplenism is a common manifestation of
portal hypertension
• The two major consequences of portal hypertension
are ascites and varices.

Ascites
• The failure of the liver to metabolize aldestreone
increase sodium and water retention by the kidney  this
causes increase intravascular volume and decrease
synthesis of albumin by the damage liver  (because of
the reduced plasma albumin concentration the patient
develop edema)
Ascites…
• Increased pressure in the portal system, forces serum proteins in to the

peritoneal cavity  Proteins draw plasma from circulating blood by
osmosis

• The kidney respond to decrease in blood volume and renal blood
pressure initiating the rennin- angiotensin aldosterone system  the
body conserves sodium ions

• Fluid retention  ascites formation in the abdomen
• Increased abdominal girth and rapid weight gain are

common presenting symptoms of ascites.
• Shortness of breath and uncomfortable from the
enlarged abdomen, and distended veins may be
visible over the abdominal wall.
• Fluid and electrolyte imbalances are common.

• The presence and extent of ascites are assessed by
percussion of the abdomen.
• The presence of fluid can be confirmed either by
percussing for shifting dullness or by detecting a fluid
wave.
• Daily measurement and recording of abdominal girth and
body weight are essential to assess the progression of
ascites
Medical Management
• The goal of treatment for the patient with ascites is a
negative sodium balance to reduce fluid retention.
• Use of diuretics along with sodium restriction is
successful in 90% of patients with ascites.
• Ammonium chloride and acetazolamide (Diamox) are
contraindicated because of the possibility of precipitating
hepatic coma.
• Paracentesis is the removal of fluid (ascites) from the
peritoneal cavity.

• Bed rest: In patients with ascites, an upright posture is
associated with activation of the renin–angiotensin–
aldosterone system and sympathetic nervous system
• This causes reduced renal glomerular filtration and
sodium excretion and a decreased response to loop
diuretics.
Nursing Management
• 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.

• 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.
• Additional patient and family teaching addresses skin
care and the need to weigh the patient daily and to watch
for and report signs and symptoms of complications.

Esophageal Varices
• Varices are varicosities that develop from elevated
pressure in the veins that drain into the portal system.
• They are prone to rupture and often are the source of
massive hemorrhages from the upper GI tract and the
rectum.

Esophageal Varices…
• Once esophageal varices form, they increase in size
and eventually bleed, in cirrhosis, they are the most
significant source of bleeding.
• The first bleeding episode has a mortality rate of
30% to 50% and is one of the major causes of death
in patients with cirrhosis.

Pathophysiology
• Esophageal varices are dilated, tortuous veins that are

usually found in the submucosa of the lower
esophagus but may develop higher in the esophagus
or extend into the stomach.
• This condition is almost always caused by portal
hypertension.

Pathophysiology…
• Because of increased obstruction of the portal vein,
venous blood from the intestinal tract and spleen seeks
an outlet through collateral circulation (new pathways
for return of blood to the right atrium).
• The effect is increased pressure, particularly in the
vessels in the submucosal layer of the lower esophagus
and upper part of the stomach.
Pathophysiology…
• Less common causes of varices are abnormalities of

the circulation in the splenic vein or superior vena
cava and hepatic venothrombosis.
• Bleeding esophageal varices are life-threatening and
can result in hemorrhagic shock that produces
decreased cerebral, hepatic, and renal perfusion.

Pathophysiology…
• Factors that contribute to hemorrhage are muscular
exertion from lifting heavy objects; straining at stool;
sneezing, coughing, or vomiting; esophagitis;
irritation of vessels by poorly chewed foods or
irritating fluids; and reflux of stomach contents
(especially alcohol).
• The patient with bleeding esophageal varices may

present with hematemesis, general deterioration in
mental or physical status and often has a history of
alcohol abuse.
• Signs and symptoms of shock (cool, clammy skin,
hypotension, tachycardia) may be present.

Endoscopy:
• Immediate endoscopy is indicated to identify the
cause and the site of bleeding; at least 30% of patients
with suspected bleeding from esophageal varices are
actually bleeding from another source (gastritis,
ulcer).

• ultrasonography, CT, and angiography.

• If the patient is actively bleeding, oral intake will not
be permitted, and the patient will be prepared for
further diagnostic and therapeutic procedures.

Laboratory Tests:
• Laboratory tests may include various liver function
tests, such as serum aminotransferases, bilirubin,
alkaline phosphatase, and serum proteins.
• Splenoportography, which involves serial or
segmental x-rays, is used to detect extensive
collateral circulation in esophageal vessels, which
would indicate varices.
• Other tests are hepatoportography and celiac
angiography.
Medical Management
• The patient requires aggressive medical care and
expert nursing care, and is usually transferred to the
intensive care unit (ICU) for close monitoring and
management.
• Vital signs are monitored continuously if
hematemesis and melena are present.
• Oxygen is administered to prevent hypoxia and to
maintain adequate blood oxygenation.

• IV fluids with electrolytes and volume expanders are
provided to restore fluid volume and replace
electrolytes.
• Transfusion of blood may be required.
• Avoid overhydration during volume resuscitation
because this would raise portal pressure and increase
bleeding.
• Nonsurgical treatment of bleeding esophageal varices
is preferable.

• Medications are administered initially like Vasopressin

(Pitressin) may be the initial mode of therapy in urgent
situations because it produces constriction of the
splanchnic arterial bed and decreases portal pressure.
• Vasopressin constricts distal esophageal and proximal
gastric veins, thus reducing the inflow into the portal
system and therefore the portal pressure.

• Monitoring of fluid intake and output and electrolyte

levels is necessary because hyponatremia may
develop and vasopressin may have an antidiuretic
effect.
• Coronary artery disease is a contraindication to the
use of vasopressin because coronary vasoconstriction
is a side effect that may precipitate myocardial
infarction.

• Somatostatin and octreotide (Sandostatin) have been

reported to be effective in decreasing bleeding from
esophageal varices.
• Beta-blocking agents like propranolol and nadolol
that decrease portal pressure, are the most common
medications used both to prevent a first bleeding
episode in patients with known varices and to prevent
rebreeding.

• In endoscopic sclerotherapy, also referred to as
injection sclerotherapy, a sclerosing agent is injected
through a fiberoptic endoscope into the bleeding
esophageal varices to promote thrombosis and eventual
sclerosis.
• The procedure has been used successfully to treat acute
GI hemorrhage but is not recommended for prevention
of first and subsequent variceal bleeding episodes.
• After treatment for acute hemorrhage, the patient must be
observed for bleeding, perforation of the esophagus,
aspiration pneumonia, and esophageal stricture.
• Antacids, histamine-2 antagonists such as cimetidine or
proton pump inhibitors may be administered after the
procedure to counteract the chemical effects of the sclerosing
agent on the esophagus and the acid reflux associated with
the therapy.
Surgical Management
• Procedures that may be used for esophageal varices are

direct surgical ligation of varices; splenorenal,
mesocaval, and portacaval venous shunts to relieve
portal pressure; and esophageal transection with
devascularization

Nursing Management
• Monitoring the patient’s physical condition and

evaluating emotional responses and cognitive status.
• Monitoring and recording vital signs and assesses the
patient’s nutritional and neurologic status.
• Gastric suction usually is initiated to keep the
stomach as empty as possible and to prevent straining
and vomiting.
• The nurse provides support and explanations about
medical and nursing interventions.

Hepatic encephalopathy and coma
• A life treating complication of liver disease,
and it is due to the accumulation of ammonia
and other toxic metabolites in the blood.
• Hepatic coma represents the most advanced
stage of hepatic encephalopathy

Hepatic encephalopathy…
• Normally ammonia forms in the intestine by
bacterial action on ingested protein, the liver
normally detoxify ammonia by converting it to
urea, which the kidneys then excrete in urine

Hepatic encephalopathy…
• But, when there is damage to liver cells  The liver fail

to detoxify and converts ammonia to urea  then,
ammonia enters the blood stream as a result of its
absorption from the GI and its liberation from kidney and
muscle cells  once, ammonia enters to the circulation,
then there will be brain dysfunction and damage  The
patient then, develop the so called Hepatic
encephalopathy

Hepatic encephalopathy and…

Patient may present with mental change and motor
disturbance, change of sleep pattern and asterixis
(flapping tremor of the hands) and sulfurous breath odor
(fetor hepaticus) may occur, they also have inability to
draw a simple figure
• When the condition is worsen the deep tendon reflux
will disappear and the extremities may become flaccid
Drawing Tests

Hepatic encephalopathy and…
• Symptoms usually worsen after the client eats a high-protein
meal or has active GI bleeding, because both dietary protein
and digested blood cells increase ammonia volume in the
intestine
Management
• Lactulose(cephulac) is administered to reduce the ammonia
– The drug can be administered by nasogastric tube or by
enema.
• IV administration of glucose to minimize protein
breakdown, administration of vitamins to correct
deficiencies, and correction of electrolyte imbalances.
• Neomycin, metronidazole (Flagyl), and rifaximin
(Xifaxan) have been used to reduce levels of ammonia-
forming bacteria in the colon.
• Patients and families are advised about foods that are
high in protein.
Nursing Management
• Maintaining a safe environment to prevent injury,
bleeding, and infection.
• Administers the prescribed treatments and monitors
the patient for the numerous potential complications.
• Encourages deep breathing and position changes to
prevent the development of atelectasis, pneumonia,
and other respiratory complications.
• Fluid intake and output and body weight are recorded each
day.
• Vital signs are measured and recorded every 4 hours.
• Neurologic status is assessed frequently.
• Reduction in the absorption of ammonia from the GI tract
is accomplished by the use of gastric suction, enemas, or
oral antibiotics.

• Vegetable protein intake may result in improved

nitrogen balance without precipitating or advancing
hepatic encephalopathy
• If the patient has recovered from hepatic
encephalopathy and is to be discharged home, the nurse
instructs the family to watch for subtle signs of
recurrent encephalopathy.
THANK YOU

Hepatitis: - Defined As

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Hepatitis: - Defined As

Uploaded by

Copyright:

Available Formats

HEPATITIS

• Defined as inflammation of the liver and characterized

Prepared by :Fikiru Y(MSc)

Prepared by :Fikiru Y(MSc)

• Viral hepatitis is a systemic viral infection in

Prepared by :Fikiru Y(MSc)

morbidity and prolonged loss of time from school or

• Hepatitis A is responsible for 37% of all cases, and

hepatitis B is the offending agent in 18% of cases.

Prepared by :Fikiru Y(MSc)

• In particular, types B and C lead to chronic disease in

hundreds of millions of people and, together, are the

most common cause of liver cirrhosis and cancer.

• Hepatitis A and E are similar in mode of transmission

• Hepatitis B, C, and D share many characteristics.

• Hepatitis A, formerly called infectious hepatitis, is

Prepared by :Fikiru Y(MSc)

• Most patients recover from hepatitis A; it rarely

progresses to acute liver necrosis or fulminant hepatitis

resulting in cirrhosis of the liver or death.

• The mortality rate of hepatitis A is approximately 1%

to 2% for older people.

Prepared by :Fikiru Y(MSc)

• Constitutional symptoms 1–2 weeks preceding the

Prepared by :Fikiru Y(MSc)

• Indigestion is present in varying degrees, marked by

• Symptoms may be mild in children; in adults, they may

Prepared by :Fikiru Y(MSc)

onset; other than jaundice, there are few other physical

• Serum alanine aminotransferase (ALT), Serum aspartate

aminotransferase (AST), Serum alkaline phosphatase

(ALP) level may be normal or only mildly elevated.

• HAV antibodies are detectable in the serum, but

usually not until symptoms appear.

• Detection of IgM anti-HAV during acute illness,

which disappears 3-6 months latter.

• Increased Serum bilirubin.

Prepared by :Fikiru Y(MSc)

• Jaundice is usually visible in the sclera or skin when

Prepared by :Fikiru Y(MSc)

Prepared by :Fikiru Y(MSc)

• Supportive care like bed rest during the acute stage

Prepared by :Fikiru Y(MSc)

• HBV is a small, double-shelled virus in the family

Prepared by :Fikiru Y(MSc)

• An estimated 2 billion persons worldwide have been

Prepared by :Fikiru Y(MSc)

Prepared by :Fikiru Y(MSc)

• Clinically, the disease closely resembles hepatitis A, but

• HBsAg is the most commonly used test for diagnosing

• HBeAg is the next antigen of HBV to appear in the

• IgM anti-HBc appears in persons with acute disease

Prepared by :Fikiru Y(MSc)

Prepared by :Fikiru Y(MSc)

Prepared by :Fikiru Y(MSc)

• The goals of treatment are to minimize infectivity and

Prepared by :Fikiru Y(MSc)

• Interferon must be administered by injection and has

Prepared by :Fikiru Y(MSc)

• Adequate nutrition should be maintained.

Prepared by :Fikiru Y(MSc)

• Hepatitis C can be developed by infection with the