 Hepatic Encephalopathy and Coma excessive diuresis, dehydration, infections, surgery,

fever, and certain medications (sedatives, tranquilizers,

Hepatic encephalopathy (HE) is a neurological syndrome
analgesics, and diuretics that cause potassium loss).
that can occur as a complication of liver disease. It is
Elevated levels of serum manganese can also contribute
characterized by a range of neuropsychiatric
to hepatic encephalopathy, as well as changes in the
abnormalities that result from the liver's inability to
types of circulating amino acids, mercaptans, and levels
detoxify substances, particularly ammonia, which then
of dopamine and other neurotransmitters in the central
affects the brain. If left untreated or if the underlying
nervous system. Mercaptans are toxic metabolites of
liver condition worsens, hepatic encephalopathy can
sulfur-containing compounds that are normally
progress to a more severe stage, leading to coma.
excreted by the liver. However, with defective hepatic

📍 PATHOPHYSIOLOGY
clearance, mercaptans and other “false”
neurotransmitters may accumulate and precipitate
encephalopathy.
The precise pathophysiology of hepatic encephalopathy

📍 CLINICAL MANIFESTATION
is not fully understood, but two major alterations
contribute to its development in acute and chronic liver
disease. Firstly, hepatic insufficiency may lead to
The earliest symptoms of hepatic encephalopathy
encephalopathy due to the liver’s inability to detoxify
include mental status changes and motor disturbances.
toxic by-products of metabolism. Secondly,
The patient appears confused and unkempt as hepatic
portosystemic shunting, resulting from collateral vessel
encephalopathy progresses, the patient may exhibit
formation due to portal hypertension, allows
alterations in mood and sleep patterns, sleeping during
substances from portal blood, typically detoxified by the
the day and experiencing restlessness and insomnia at
liver, to enter the systemic circulation. Ammonia is
night. They may become difficult to awaken and
considered the major factor in encephalopathy
disoriented regarding time and place. In advanced
development. It enters the brain, stimulating
stages, the patient may lapse into coma and may
neurotransmission pathways that lead to CNS
experience seizures. Asterixis, characterized by
depression, inhibiting synaptic regulation and causing
involuntary flapping of the hands, may be observed in
the behavioral and sleep patterns associated with
stage II encephalopathy. Simple tasks like handwriting
hepatic encephalopathy.
may become difficult, and constructional apraxia, the
Circumstances that increase serum ammonia levels tend inability to reproduce simple figures, may occur. Deep
to aggravate or precipitate hepatic encephalopathy. The tendon reflexes are initially hyperactive but may
largest source of ammonia is the enzymatic and disappear as encephalopathy worsens, leading to flaccid
bacterial digestion of dietary and blood proteins in the extremities.
GI tract. Ammonia levels can increase due to factors
Occasionally, fetor hepaticus, characterized by a sweet,
such as GI bleeding (e.g., bleeding esophageal varices,
slightly fecal odor to the breath, may be observed. This
chronic GI bleeding), a high-protein diet, bacterial
odor is believed to originate from the intestines and has
infection, or uremia. Additionally, ingestion of
been described as similar to the smell of freshly mowed
ammonium salts can elevate blood ammonia levels. In
grass, acetone, or old wine. Fetor hepaticus is
the presence of alkalosis or hypokalemia, increased
commonly associated with extensive collateral portal
amounts of ammonia are absorbed from the GI tract
circulation in chronic liver disease.
and renal tubular fluid.

Conversely, serum ammonia levels can be decreased by
eliminating protein from the diet and by administering
antibiotics such as neomycin sulfate, which reduce the
number of intestinal bacteria capable of converting urea
to ammonia. Other factors unrelated to increased
serum ammonia levels that can cause hepatic
encephalopathy in susceptible patients include
📍 ASSESSMENT AND DIAGNOSTIC FINDINGS
Several diagnostic algorithms and various psychometric
tests are utilized to determine the presence and
severity of hepatic encephalopathy.
Electroencephalogram findings typically reveal
generalized slowing, increased brain wave amplitude,
and characteristic triphasic waves. Following the first
episode of overt hepatic encephalopathy in patients
with cirrhosis, the survival rate is approximately 40% at
1 year. Eligible patients should be referred for liver
transplantation after this initial episode.
📍MEDICAL MANAGEMENT
Medical management of hepatic encephalopathy
focuses on identifying and addressing the precipitating
cause, initiating ammonia-lowering therapy, minimizing
potential medical complications of cirrhosis and
depressed consciousness, and reversing the underlying
liver disease if possible. Correction of potential reasons
for deterioration such as bleeding, electrolyte
abnormalities, sedation, or azotemia is crucial.
Lactulose is administered to reduce serum ammonia
levels by trapping and expelling ammonia in the feces.
The goal is to achieve two or three soft stools per day,
indicating effective lactulose therapy.
Possible side effects of lactulose include intestinal
bloating and cramps, typically resolving within a week.
To mitigate the sweet taste, which some patients find
unpleasant, it can be diluted with fruit juice. Close
monitoring for hypokalemia and dehydration is
essential. Other laxatives are avoided during lactulose
administration to maintain dosage regulation. In
comatose patients or those unable to take oral
medication, lactulose may be administered via
nasogastric tube or enema. Additional management
strategies include IV glucose administration to minimize
protein breakdown, vitamin supplementation to correct
deficiencies, and correction of electrolyte imbalances,
particularly potassium. Antibiotics such as neomycin,
metronidazole, and rifaximin may be used to reduce
levels of ammonia-forming bacteria in the colon.
However, long-term treatment with antibiotics such as
neomycin, metronidazole, and rifaximin has not been
shown to provide benefit. Additional management
strategies for hepatic encephalopathy include frequent
assessment of neurologic status, monitoring mental
status by recording daily handwriting and arithmetic
performance, recording intake and output and body
weight daily, measuring and recording vital signs every
4 hours, frequent assessment for potential sites of
infection and prompt reporting of abnormal findings,
daily monitoring of serum ammonia levels, and ensuring
adequate dietary protein intake, maintained at 1.2 to
1.5 g/kg/day. Enteral feeding may be provided for
patients with persistent encephalopathy. Reduction in
ammonia absorption from the GI tract can be achieved
through gastric suction, enemas, or oral antibiotics.
Electrolyte status is monitored and corrected if
abnormal, and sedatives, tranquilizers, and analgesic
medications are discontinued. IV administration of
benzodiazepine antagonists such as flumazenil may be
used to improve encephalopathy, regardless of previous
benzodiazepine use, with potential short-term efficacy
due to increased benzodiazepine receptor
concentration in patients with hepatic encephalopathy.
📍NURSING MANAGEMENT
Presents the stages of hepatic encephalopathy,
common signs and Symptoms, and potential nursing
diagnoses for each stage. The nurse is Responsible for
maintaining a safe environment to prevent injury,
bleeding, and Infection. The nurse administers the
prescribed treatments and monitors the Patient for the
numerous potential complications. The potential for
respiratory Compromise is great given the patient’s
depressed neurologic status. The nurse Encourages
deep breathing and position changes to prevent the
development of Atelectasis, pneumonia, and other
respiratory complications. Despite Aggressive
pulmonary care, patients may develop respiratory
compromise. They may require intubation and
mechanical ventilation to protect the airway, And they
are frequently admitted to the ICU. The nurse
communicates with the patient’s family to inform them
about the Patient’s status and supports them by
explaining the procedures and treatments That are part
of the patient’s care. If the patient recovers from
hepatic Encephalopathy and coma, rehabilitation is
likely to be prolonged. Therefore, The patient and
family will require assistance to understand the causes
of this Severe complication and to recognize that it may
recur.
OTHER MANIFESTATIONS OF HEPATIC DYSFUNCTION
EDEMA AND BLEEDING
Edema and bleeding
Edema and bleeding are two significant manifestations
of various medical conditions, each with distinct
underlying causes and management approaches.
Edema: specialists, is crucial for providing comprehensive care
to patients experiencing these symptoms.
Definition: Edema refers to the abnormal accumulation
of fluid in the interstitial spaces, leading to swelling in VITAMIN DEFICIENCY
various parts of the body.
The decreased production of clotting factors may be
Causes: Edema can result from several factors, including linked to deficient absorption of vitamin K from the GI
heart failure, kidney disease, liver disease, venous tract, possibly due to the liver cells’ inability to utilize
insufficiency, inflammation, and certain medications. vitamin K for prothrombin synthesis (Barrett et al.,
2019; Hammer & McPhee, 2019). Additionally, impaired
Manifestations: Common signs of edema include
absorption of other fat-soluble vitamins (A, D, and E)
swelling, puffiness, and tightness of the affected area,
and dietary fats could occur due to reduced secretion of
which can be localized or generalized.
bile salts into the intestine
Management: Treatment aims to address the
In severe chronic liver dysfunction, decreased secretion
underlying cause of edema. This may involve diuretic
of bile salts into the intestine can lead to various
medications to reduce fluid retention, lifestyle
problems, including inadequate intake of essential
modifications such as sodium restriction, elevation of
vitamins. These deficiencies manifest as:
the affected limbs, compression therapy, and
management of any contributing conditions. Vitamin A deficiency: causing night blindness and skin
changes.
Bleeding:
Thiamine deficiency: leading to beriberi, polyneuritis,
Definition: Bleeding refers to the escape of blood from
and Wernicke–Korsakoff psychosis.
the circulatory system, which can occur internally or
externally. Riboflavin deficiency: resulting in characteristic skin and
mucous membrane lesions.
Causes: Bleeding can result from various factors,
including trauma, surgery, gastrointestinal ulcers, Pyridoxine deficiency: causing skin and mucous
hemorrhagic disorders, anticoagulant medications, and membrane lesions and neurologic changes.
vascular abnormalities.
Vitamin C deficiency: resulting in hemorrhagic lesions of
Manifestations: Symptoms of bleeding vary depending scurvy.
on the site and severity of the bleed but may include
Vitamin K deficiency: leading to hypoprothrombinemia,
visible blood loss, bruising, petechiae, hematomas,
characterized by spontaneous bleeding and
melena (black, tarry stools), hematuria (blood in urine),
ecchymoses.
and hematemesis (vomiting blood).
Folic acid deficiency: resulting in macrocytic anemia.
Management: Management of bleeding depends on its

📍 METABOLIC ABNORMALITIES
cause and severity. Immediate interventions may
include applying direct pressure to the bleeding site,
administering blood products or clotting factors,
surgical intervention, and medication adjustments (e.g., Abnormalities of glucose metabolism also occur; the
stopping anticoagulants). Long-term management may blood glucose level may
involve addressing underlying conditions, such as Be abnormally high shortly after a meal (similar to that
treating ulcers or managing coagulation disorders, to when diabetes is
prevent recurrence.
Present), but hypoglycemia may occur during fasting
In summary, edema and bleeding are both significant because of decreased
clinical manifestations that require thorough
assessment, accurate diagnosis, and appropriate Hepatic glycogen reserves and decreased
management to address the underlying causes and gluconeogenesis. Medications must
prevent complications. Collaboration among healthcare
professionals, including nurses, physicians, and
Be used cautiously and in reduced dosages because the
ability to metabolize
Medications is decreased in the patient with liver
failure.
Liver dysfunction can lead to various endocrine
abnormalities due to impaired hormone metabolism,
including androgens and sex hormones. When the liver
fails to inactivate estrogens properly, it can result in
gynecomastia, amenorrhea, testicular atrophy, loss of
pubic hair in males, menstrual irregularities in females,
and other disruptions of sexual function and
characteristics.
📍 PRURITUS AND OTHER SKIN CHANGES
Patients with liver dysfunction due to biliary obstruction
often experience severe pruritus caused by bile salt
retention. Additionally, they may develop vascular
spider angiomas on the skin, typically above the
waistline, resembling spider legs. These angiomas are
commonly associated with cirrhosis, especially in
alcoholic liver disease. Palmar erythema, characterized
by reddened palms, may also occur in these patients
📍VIRAL HEPATITIS
Viral hepatitis is a systemic infection characterized by
necrosis and inflammation of liver cells, resulting in
distinct clinical, biochemical, and cellular changes. There
are five definitive types: hepatitis A, B, C, D, and E.
Hepatitis A and E are transmitted via the fecal-oral
route, while hepatitis B, C, and D share many other
characteristics
Hepatitis is easily transmitted and can lead to significant
morbidity and prolonged absence from school or work.
Acute viral hepatitis affects approximately 0.5% to 1% of
people in the United States each year. In 2017, hepatitis
A virus (HAV) was responsible for 3366 cases in the
United States. Although incidence rates decreased by
more than 95% from 1995 to 2011, there was a
subsequent increase of 140% from 2011 to 2017.
Notably, in 2017, large person-to-person outbreaks
began occurring among individuals who use drugs and
those experiencing homelessness (Centers for Disease
Control and Prevention [CDC], 2017).In 2017, the
hepatitis B virus (HBV) caused a total of 3407 cases of
acute viral hepatitis across the nation. The incidence
rate of hepatitis C virus (HCV) in the same year was
3186 cases, with an incidence of 1.0 case per 100,000
population, indicating an increase since 2013.
📍 HEPATITIS A VIRUS
Hepatitis A virus (HAV) accounts for approximately 20%
to 25% of clinical hepatitis cases in the United States
(CDC, 2017). Formerly known as infectious hepatitis,
hepatitis A is caused by an RNA virus of the enterovirus
family. In the U.S., the disease primarily affects the
adult population. HAV is transmitted primarily through
the fecal-oral route, typically via the ingestion of
contaminated food or liquids. It is more common in
regions with overcrowding and poor sanitation. The
virus can be detected in the stool of infected individuals
before the onset of symptoms and during the early days
of illness.
Hepatitis A infection is often acquired by children or
young adults at school through poor hygiene practices,
hand-to-mouth contact, or close contact with an
infected individual. The virus can then spread within
families due to inadequate sanitary habits. Additionally,
transmission can occur through infected food handlers
or consumption of contaminated water or shellfish.
Outbreaks have been observed in day care centers and
institutions, particularly among individuals with
developmental disabilities, due to poor hygiene
practices. Hepatitis A can also be transmitted through
sexual activity, especially through oral-anal contact or
anal intercourse and with multiple sex partners.
Notably, hepatitis A is not transmitted through blood
transfusions.
The incubation period for hepatitis A is typically
between 2 and 6 weeks, with an average of around 4
weeks (CDC, 2017; Chi et al., 2018; Shin & Jeong, 2018).
The illness can last for 4 to 8 weeks and tends to be
more severe and prolonged in individuals over 40 years
old. While most patients recover from hepatitis A, it
rarely progresses to acute liver necrosis or hepatic
failure leading to cirrhosis or death. The mortality rate
of hepatitis A is approximately 0.5% for individuals
younger than 40 years and 1% to 2% for older adults. In
individuals with underlying chronic liver disease, the risk
of morbidity and mortality is increased during acute
hepatitis A infection.There is no carrier state or chronic
hepatitis associated with hepatitis A virus (HAV), and
the virus is present in the serum only briefly. By the
time jaundice develops, the patient is likely
noninfectious. Although hepatitis A provides immunity
against itself, individuals can still contract other forms
of hepatitis.
available, providing 95% to 100% protection after two
to three doses (Link-Gelles, Hofmeister, & Nelson,
2018). It is recommended that adults aged 18 years and
older receive the two-dose vaccine, with the second
dose administered 6 to 12 months after the first.

📍 CLINICAL MANIFESTATION
Protection against HAV typically develops within several
weeks after the initial dose of the vaccine.

Children and adolescents aged 1 to 18 years typically

Many patients with hepatitis A are asymptomatic and
receive three doses of the hepatitis A vaccine. The
do not develop jaundice. When symptoms do occur,
second dose is administered one month after the first,
they often resemble those of a mild flu-like upper
and the third dose is given 6 to 12 months later. Routine
respiratory tract infection, with low-grade fever.
immunization of young children with the hepatitis A
Anorexia is an early and often severe symptom, possibly
vaccine has proven effective in reducing disease
resulting from the release of toxins by the damaged
incidence and maintaining low levels across all age
liver or the failure of damaged liver cells to detoxify
groups in many settings (Chi et al., 2018; Goldman &
abnormal products. Jaundice and dark urine may
Schafer, 2019).
become apparent later in the course of the illness.
For individuals who have not been previously
Patients with hepatitis A may experience varying
vaccinated against hepatitis A virus (HAV), prevention
degrees of symptoms, typically marked by vague
can be achieved through intramuscular administration
epigastric distress, nausea, heartburn, and flatulence.
of immune globulin during the incubation period, if
Additionally, they may develop a strong aversion to the
given within 2 weeks of exposure. This helps boost
taste of cigarettes or the presence of cigarette smoke
antibody production and provides 6 to 8 weeks of
and other strong odors (Papadakis & McPhee, 2020;
passive immunity. Immune globulin may also suppress
Shin & Jeong, 2018). These symptoms often improve as
overt symptoms of the disease, resulting in a subclinical
jaundice reaches its peak, usually around 10 days after
case of HAV that still produces immunity to subsequent
its initial appearance. While symptoms may be mild in
episodes of the virus.
children, they tend to be more severe and prolonged in

📍 MEDICAL MANAGEMENT
adults.

📍 ASSESSMENT AND DIAGNOSTIC FINDINGS During the acute stage of hepatitis A, bed rest and a
nutritious diet are crucial aspects of treatment. Patients
After the onset of hepatitis A, the liver and spleen may
experiencing anorexia should receive frequent small
be moderately enlarged for a few days, with few other
feedings, possibly supplemented with IV fluids
physical signs aside from jaundice. HAV antigen may be
containing glucose if necessary. Given the patient’s
present in the stool 7 to 10 days before illness and for 2
potential aversion to food, gentle persistence and
to 3 weeks after symptoms appear. HAV antibodies are
creativity may be needed to stimulate appetite.
detectable in the serum, typically not until symptoms
Maintaining optimal food and fluid intake is essential to
appear. Subclass analysis of immunoglobulins can help
counteract weight loss and expedite recovery. Many
differentiate between acute and past infections.
patients regain their appetites even before the onset of

📍 PREVENTION
Several strategies can help prevent the transmission of
hepatitis A virus (HAV). Patients and their families are
advised to follow general precautions such as
jaundice. The patient’s sense of well-being and
laboratory test results typically guide decisions
regarding bed rest and physical activity restriction.
Gradual but progressive ambulation can help accelerate
recovery.

📍 PREVENTION OF HEPATITIS
maintaining scrupulous hand hygiene, ensuring safe
water supplies, and proper control of sewage disposal.
Additionally, highly effective and safe HAV vaccines are
Prevention strategies for hepatitis include:
Vaccination: Highly effective and safe hepatitis A
vaccines are available for both adults and children.
Routine immunization of young children and expanded
recommendations for vaccination in high-risk groups
have contributed to a significant reduction in disease
incidence.
Improved hygiene: Encouraging scrupulous hand
hygiene, safe water supplies, and proper sewage
disposal can help prevent transmission of hepatitis A
virus.
Immune globulin administration: For individuals not
previously vaccinated, administration of immune
globulin during the incubation period, if given within 2
weeks of exposure, can provide temporary passive
immunity against hepatitis A.
Nutritious diet and bed rest: During the acute stage of
hepatitis A, bed rest and a nutritious diet, including
frequent small feedings and possibly IV fluids with
glucose supplementation, are important for recovery.
Monitoring and management: Regular monitoring of
patient well-being and laboratory test results guides
decisions regarding bed rest and physical activity.
Gradual ambulation can aid in recovery.
Overall, a combination of vaccination, hygiene practices,
and supportive care plays a key role in preventing
hepatitis A infection and promoting recovery in affected
individuals.
📍 NURING MANAGEMENT
Management of hepatitis A typically occurs at home
unless symptoms are severe. In such cases, the nurse
assists the patient and family in coping with the
temporary disability and fatigue commonly associated
with hepatitis A virus (HAV). Education is provided on
seeking additional healthcare if symptoms persist or
worsen. Patients and families receive specific guidelines
regarding diet, rest, follow-up blood work, and the
importance of abstaining from alcohol. They are also
instructed on sanitation and hygiene measures,
particularly emphasizing hand hygiene, to prevent the
spread of the disease to other family members.
Education for patients and families includes:
Good personal hygiene: Emphasizing careful
handwashing to reduce the risk of contracting hepatitis
A.
Dietary recommendations: Providing guidance on a
nutritious diet and frequent small feedings to support
recovery.
Rest: Advising adequate rest to aid in recovery and
reduce fatigue.
Follow-up care: Stressing the importance of follow-up
blood work to monitor liver function and overall health.
Avoidance of alcohol: Educating on the importance of
abstaining from alcohol consumption to support liver
health and healing.
📍 HEPATITIS B VIRUS
Unlike HAV, the 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. HBV is also transferred from carrier
mothers to their
Infants, especially in areas with a high incidence (e.g.,
Southeast Asia). The
Infection usually is not transmitted via the umbilical
vein but from the mother
At the time of birth and during close contact afterward.
HBV has a long incubation period. It replicates in the
liver and remains in
The serum for relatively long periods, allowing
transmission of the virus. Risk
Factors for HBV infection are summarized in Chart 43-7.
Screening of blood
Donors has greatly reduced the occurrence of HBV after
blood transfusion.
📍 GERONTOLOGIC CONSIDERATION
The immune system undergoes changes in older adults,
leading to decreased responsiveness. This may
contribute to the increased incidence and severity of
hepatitis B virus (HBV) infection among older
individuals, as well as an increased incidence of liver
abscesses due to decreased phagocytosis by Kupffer
cells. Older patients with HBV face a serious risk of
severe liver cell necrosis or acute hepatic failure,
especially when other illnesses are present. However,
the widespread use of HBV vaccines for prevention may
lead to a decrease in the incidence of hepatic diseases
in the future.
📍CLINICAL MANIFESTATION
Hepatitis B virus (HBV) clinically resembles hepatitis A
virus (HAV), but it has a much longer incubation period
of 1 to 6 months. Signs and symptoms of HBV infection
can be insidious and variable. Fever and respiratory
symptoms are rare, while some patients may
experience arthralgias and rashes. Common symptoms
include loss of appetite, dyspepsia, abdominal pain,
generalized aching, malaise, and weakness. Jaundice
may or may not be present, but if it occurs, it is
accompanied by light-colored stools and dark urine. The
liver may be tender and enlarged, typically reaching 12
to 14 cm vertically. Enlargement of the spleen and
palpable posterior cervical lymph nodes may also occur
in some patients. Subclinical episodes are also common
with HBV infection.
📍 ASSESSMENT AND DIAGNOSTIC FINDINGS
Hepatitis B virus (HBV) is a deoxyribonucleic acid (DNA)
virus composed of the following antigenic particles:
HBcAg: Hepatitis B core antigen, which is antigenic
material located in an inner core.
HBsAg: Hepatitis B surface antigen, which is antigenic
material on the viral surface and serves as a marker of
active replication and infection.
HBeAg: An independent protein circulating in the blood.
HBxAg: Gene product of the X gene of HBV DNA.
Each antigen elicits its specific antibody and serves as a
marker for different stages of the disease process:
Anti-HBc: Antibody to the core antigen of HBV; persists
during the acute phase of illness and may indicate
continuing HBV presence in the liver.
Anti-HBs: Antibody to surface determinants on HBV;
detected during late convalescence and usually
indicates recovery and development of immunity.
Anti-HBe: Antibody to hepatitis B e-antigen; usually
signifies reduced infectivity.
Anti-HBxAg: Antibody to the hepatitis B x-antigen; may
indicate ongoing replication of HBV.
📍 PREVENTION
Prevention of hepatitis B transmission requires a
multifaceted approach,
Including public health interventions and education as
well as programs to
Foster immunization against this virulent virus in an
effort to reduce the disease
Burden.
📍PREVENTING TRANSMISSION
Continued screening of blood donors for the presence
of hepatitis B antigen (HBsAg) further reduces the risk
of transmission through blood transfusion. The
adoption of disposable syringes, needles, and lancets, as
well as the implementation of needleless IV
administration systems, has significantly decreased the
risk of spreading the infection from one patient to
another or to healthcare personnel during blood sample
collection or parenteral therapy administration. In
clinical laboratories and hemodialysis units, work areas
are disinfected daily, and gloves are worn when
handling all blood and body fluids, including HBsAg-
positive specimens, or when there is potential exposure
to blood, such as during blood drawing or when
handling patients’ secretions.Eating is prohibited in
areas exposed to secretions, blood, or blood products.
Patient education about the nature of the disease, its
infectiousness, and prognosis is crucial for preventing
transmission and protecting contacts.
📍ACTIVE IMMUNIZATION: HBV
Active immunization against hepatitis B virus (HBV) is
recommended for individuals at high risk, such as
healthcare personnel and patients undergoing
hemodialysis. Additionally, individuals with hepatitis C
virus (HCV) and other chronic liver diseases should
receive the vaccine. In 2018, the Advisory Committee on
Immunization Practices (ACIP) recommended the use of
a newly licensed hepatitis B vaccine, HEPLISAV-B, for
individuals over the age of 18. This vaccine is
administered in two doses given 1 month apart,
potentially increasing completion rates of the full
vaccine series.Previously, a yeast-recombinant hepatitis
B vaccine was used to provide active immunity and has
shown protection rates greater than 90% in healthy
individuals. Although antibody levels may decline over
time, immunologic memory may persist for at least 5 to
10 years, and measurable antibody levels may not be
necessary for protection. In individuals with normal
immune systems, booster doses are generally not
required, but they may be recommended for
immunocompromised individuals.Rarely, a hepatitis B
vaccine prepared from plasma of humans chronically
infected with HBV is used in patients who are
immunodeficient or allergic to recombinant yeast-
derived vaccines.
People at high risk, including nurses and other
healthcare personnel exposed to blood or blood
products, should receive active immunization against
hepatitis B virus (HBV). Healthcare workers with
frequent blood contact are screened for anti-HBs to
determine if immunity is already present from prior
exposure. The vaccine provides active immunity to HBV
in 90% to 95% of healthy individuals and does not
protect against other types of viral hepatitis or provide
protection to those already exposed to HBV.Given the
sexual transmission of HBV, vaccination is
recommended for individuals being evaluated for
sexually transmitted infections (STIs), those with a
history of an STI, individuals with multiple sex partners,
individuals who have sex with people who use injection
drugs, and men who are sexually active with other men.
📍PASSIVE IMMUNITY: HEPATITIS B IMMUNE GLOBULIN
Hepatitis B immune globulin (HBIG) provides passive
immunity to hepatitis B virus (HBV) and is indicated for
individuals exposed to HBV who have never had
hepatitis B and have never received hepatitis B vaccine.
Specific indications for postexposure prophylaxis with
HBIG include inadvertent exposure to HBsAg-positive
blood through percutaneous (needlestick) or
transmucosal (splashes in contact with mucous
membrane) routes, sexual contact with HBsAg-positive
individuals, and perinatal exposure (infants born to
HBV-infected mothers should receive HBIG within 12
hours after delivery). HBIG is prepared from plasma
selected for high titers of anti-HBs antibodies.
Prompt administration of HBIG (within hours to a few
days after HBV exposure) increases the likelihood of
protection. Both active and passive immunization are
recommended for individuals exposed to HBV through
sexual contact or percutaneous or transmucosal routes.
If HBIG and hepatitis B vaccines are administered
simultaneously, separate injection sites and syringes
should be used. HBIG is considered very safe, with no
evidence of infectious disease transmission due to its
administration.
📍MEDICAL MANAGEMENT
The goals of treating chronic hepatitis B virus (HBV)
infection are to minimize infectivity, reduce liver
inflammation, and alleviate symptoms. Among the
agents used for treatment, alpha-interferon shows the
most promise. A regimen of 5 million units daily or 10
million units three times weekly for 16 to 24 weeks can
lead to disease remission in approximately one third of
patients. Prolonged treatment may offer additional
benefits and is currently being studied.
However, alpha-interferon must be administered via
injection and is associated with significant side effects,
including fever, chills, anorexia, nausea, myalgias, and
fatigue. More serious delayed side effects such as bone
marrow suppression, thyroid dysfunction, alopecia, and
bacterial infections may necessitate dosage reduction
or discontinuation. Various recombinant forms of alpha-
interferon, including the pegylated form (peginterferon
alfa-2a), with once-weekly dosing, are also available
Pegylated interferon, particularly peginterferon alfa-2a,
with once-weekly dosing, has largely replaced standard
interferon due to its convenience. The American
Association for the Study of Liver Diseases (AASLD)
recommends pegylated interferon, entecavir, or
tenofovir as preferred initial therapy for adults with
chronic hepatitis B. Entecavir and tenofovir are oral
nucleoside analogs approved for use in chronic hepatitis

B in the United States. They are also recommended for
patients with HBV-related decompensated cirrhosis, a
condition characterized by severe liver dysfunction.
Studies have shown improved outcomes, including
increased seroconversion rates, improved liver function,
and reduced progression to cirrhosis, with the use of
entecavir and tenofovir. These agents can also be used
for patients with decompensated cirrhosis who are
awaiting liver transplantation. Decompensated cirrhosis
refers to severe liver damage resulting in life-
threatening complications such as ascites,
encephalopathy, or variceal hemorrhage.
During the acute phase of hepatitis, bed rest may be
recommended until symptoms subside, and activities
are restricted until hepatic enlargement and serum
bilirubin and liver enzyme levels have decreased.
Gradually, increased activity is allowed.
Adequate nutrition is essential, and protein intake
should not be restricted. Protein intake should be
maintained at 1.2 to 1.5 grams per kilogram per day.
Measures to alleviate dyspeptic symptoms and general
malaise may include the use of antacids and antiemetic
agents, but all medications should be avoided if
vomiting occurs. Persistent vomiting may necessitate
hospitalization and fluid therapy.
Due to the mode of transmission, the patient should be
evaluated for other bloodborne diseases, such as
human immunodeficiency virus (HIV) infection.
📍 NURSING MANAGEMENT
Convalescence from hepatitis may be prolonged, with
complete symptomatic recovery sometimes taking 3 to
4 months or longer. During this stage, gradual
resumption of physical activity is encouraged after the
resolution of jaundice.The nurse plays a crucial role in
identifying 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. Planning is necessary to minimize social
isolation, and involving the family in the planning
process can help alleviate their fears and anxieties
about the spread of the disease.
📍 PROMOTING HOME, COMMUNITY -BASED AND
TRANSITIONAL CARE
Due to the prolonged period of convalescence,
preparation for home care is essential for the patient
and family. Adequate rest and nutrition must be
ensured. The nurse educates family members and close
contacts about the risks of contracting hepatitis B virus
(HBV) and arranges for them to receive hepatitis B
vaccine or hepatitis B immune globulin (HBIG) as
prescribed. Those at risk should be informed about the
early signs of HBV and ways to reduce risk by avoiding
all modes of transmission. Additionally, patients with all
forms of hepatitis should refrain from drinking alcohol
to support their recovery.
📍 HEPATITIS C VIRUS
Hepatitis C virus (HCV) transmission in the United States
has shifted from blood transfusions and sexual contact
to other parenteral means, such as sharing
contaminated needles among IV or injection drug users,
and unintentional needlesticks and injuries among
healthcare workers. In 2017, 3,186 cases of acute
hepatitis C were reported to the CDC, but after
adjusting for under-ascertainment and under-reporting,
an estimated 44,300 cases occurred.Approximately 2.5
million people in the United States are living with HCV,
making it the most common chronic bloodborne
infection nationally, with many infected individuals
unaware of their status. The highest prevalence of HCV
is observed among adults aged 40 to 59, with the
highest rates among African Americans in this age
group. In 2017, HCV was cited as an underlying or
contributing cause of death on 17,253 U.S. death
certificates, although it is believed that deaths from this
cause are underestimated. HCV is responsible for about
one-third of hepatocellular carcinoma (HCC) cases and
is one of the leading reasons for liver transplantation.
People at particular risk for hepatitis C virus (HCV)
include IV or injection drug users, individuals with
multiple sexual partners, patients requiring frequent
transfusions or large volumes of blood, and healthcare
personnel. The incubation period for HCV is variable,
ranging from 15 to 160 days. The clinical course of acute
HCV is usually mild or asymptomatic, similar to hepatitis
B virus (HBV). However, chronic carrier states are
common with HCV, leading to an increased risk of
 📍 HEPATITIS G VIRUS AND GB VIRUS-C
chronic liver disease, including cirrhosis or liver cancer.
Therefore, individuals in high- and moderate-risk
groups, as well as those from regions with high
It has been long suspected that there is another agent,
prevalence rates, should be screened for HCV along
distinct from hepatitis A to E, causing hepatitis in
with HBV. Regular consumption of small amounts of
humans. The incubation period for post-transfusion
alcohol may exacerbate disease progression, so alcohol
hepatitis is between 14 to 145 days, which is too long
and medications that affect the liver should be avoided.
for hepatitis B or C. Approximately 5% of chronic liver
Treatment for hepatitis C virus (HCV) infection has disease cases in the United States are cryptogenic,
advanced significantly with the introduction of highly meaning they do not appear to have autoimmune or
effective HCV protease inhibitor therapies since 2011. viral origins, and 50% of these patients have a history of
Current therapies can achieve sustained virologic blood transfusions before developing the disease. This
response (SVR), defined as the absence of detectable has led to the identification of another form of
virus 12 weeks after treatment completion, indicating a hepatitis, known as hepatitis G virus (HGV) or GB virus-C
cure of HCV infection. Over 90% of individuals infected (GBV-C), which are believed to be two different isolates
with HCV can be cured regardless of the HCV genotype, of the same virus transmitted percutaneously.
with 8 to 12 weeks of oral therapy. HCV direct-acting Autoantibodies are absent in these cases. However, the
antivirals (DAA), such as simeprevir plus sofosbuvir, clinical significance of this virus remains uncertain. Risk
ledipasvir-sofosbuvir, and ombitasvir-paritaprevir- factors for HGV/GBV-C infection are similar to those for
ritonavir with dasabuvir, have fewer side effects, hepatitis C, but there is no clear relationship between
shorter treatment durations, and higher cure rates HGV/GBV-C infection and progressive liver disease.
compared to previous antiviral agents. Another dual While persistent infection can occur, it does not
combination, which includes a derivative of daclatasvir significantly impact the clinical course.
with sofosbuvir, is equally effective against all HCV
genotypes. Prescribers must consider the degree of
cirrhosis in individual patients to determine the most
appropriate protease inhibitor. The American
Association for the Study of Liver Diseases (AASLD)
recommends specific regimens for simplified HCV
treatment for treatment-naïve adults without cirrhosis
or those with compensated cirrhosis, such as
glecaprevir/pibrentasvir or sofosbuvir/velpatasvir,
depending on the genotype.

📍 HEPATITIS E VIRUS

Hepatitis E virus (HEV) is believed to be transmitted

through the fecal-oral route, primarily via contaminated
water in areas with poor sanitation. The incubation
period varies, typically ranging from 15 to 65 days.
Hepatitis E closely resembles hepatitis A, characterized
by a self-limited course with a sudden onset. Jaundice is
almost always present, but chronic forms of the disease
do not develop. Prevention of hepatitis E primarily
involves avoiding contact with the virus through good
hygiene practices, including handwashing. The
effectiveness of immune globulin in protecting against
HEV is uncertain.