Hepatitis A

Hepatitis A
Straight to the point of care
Last updated: Feb 21, 2024

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Aetiology 5
Pathophysiology 6
Case history 6
Diagnosis 7
Approach 7
History and exam 8
Risk factors 10
Investigations 12
Differentials 13
Management 16
Approach 16
Treatment algorithm overview 18
Treatment algorithm 19
Primary prevention 21
Secondary prevention 21
Patient discussions 22
Follow up 24
Monitoring 24
Complications 25
Prognosis 26
Guidelines 27
Diagnostic guidelines 27
Treatment guidelines 28
Online resources 30
References 31
Images 36
Disclaimer 40
Hepatitis A Overview
Summary
Hepatitis A transmission usually precedes symptoms by 2 weeks, but can be up to 7 weeks, when stool viral
concentrations are highest. Patients are considered non-infectious 1 week after onset of jaundice.
OVERVIEW
Symptomatic patients may present with abrupt-onset fever, abdominal pain, malaise, jaundice, dark urine or
light-coloured stools, or diarrhoea.
Immunoglobulin M anti-hepatitis A virus serology is the test of choice for diagnosis.
Common examination findings are hepatomegaly and clinical jaundice with marked elevation of serum
transaminases (usually >1000 units/L).
No specific therapy is available, and treatment is usually supportive.
Post-exposure prophylaxis may be with active or passive immunisation, depending on specific patient factors,
and according to individual national guidelines.
Definition
Hepatitis A virus (HAV) is an RNA virus. Mode of transmission is faecal-oral. Most infections in adults and
older children are symptomatic; 70% develop jaundice. The majority of infections in children younger than 6
years are asymptomatic.[1] Average incubation period is 28 days (range 15-50 days).[1]
Unlike hepatitis B and C infections, hepatitis A infection is not associated with chronic liver disease.[1] [2]
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Feb 21, 2024.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
3
can be found on bestpractice.bmj.com . Use of this content is subject to our disclaimer (.
Use of this content is subject to our) . © BMJ Publishing Group Ltd 2024. All rights reserved.
Hepatitis A Theory
Epidemiology
Hepatitis A virus (HAV) infection is endemic in resource-limited countries.[1] In developed countries,
outbreaks are associated with contaminated food or water. Men who have sex with men, people who use
THEORY
illegal drugs, people who experience homelessness, and people who travel to endemic areas are at higher
risk of infection.[1] [5] There are an estimated 1.4 million cases per year globally.[5]
High-prevalence areas include Africa and parts of Asia and Latin America.[6] [7] [8] [9] The majority of
infections in these areas occur in early childhood; infections are often asymptomatic in children and reported
incidence rates are low. In high-prevalence areas, adults are generally immune.
Regions of Southern and Eastern Europe and parts of the Middle East have intermediate prevalence.[10]
Areas of low prevalence and very low prevalence include North America and Western Europe, where
few people are infected in childhood and the majority of the population remains susceptible throughout
adulthood.[10] [11] [12]
Geographical distribution of the prevalence of hepatitis A (based on summary of available data)

CDC website; used with permission
In the US, HAV infection continues to be one of the most frequently reported vaccine-preventable conditions.
An outbreak of HAV infection was seen in the US from 2015 to 2020. The cases started decreasing from
2020, and eight states declared the end of the outbreak in 2021. In 2021, the Centers for Disease Control
and Prevention received 11,500 reports of HAV infection from US states and territories, which is 4% higher
than that in 2015 but 43% lower than that in 2020.[13]
There have been an estimated 44,910 cases, 27,441 hospitalisations and 423 deaths following HAV infection
since the hepatitis A outbreaks were first identified in 2016.[14] In 2021, 3864 cases of hepatitis A were
reported by 30 European Economic Area countries.[15]
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Feb 21, 2024.
Hepatitis A Theory
Aetiology
Hepatitis A virus (HAV) is a 27-nm, non-enveloped, icosahedral RNA virus.[16] [17]
THEORY
An electron micrograph of the hepatitis A virus
CDC/Betty Partin; used with permission
The virus is resistant to bile lysis due to lack of a lipid envelope.[18] The virus is resistant to freezing,
detergents, and acids. It is inactivated by formalin and chlorine. The virus survives on human hands and
fomites and requires temperatures higher than 185°F (85°C) for inactivation.[19] [20] HAV survives for
extended periods in sea water, fresh water, waste water, and soil.[19] The virus is transmitted by close
contact with an infected person or by contact with contaminated food or water products.
Children are a key source of HAV infection in developing countries. Infection is frequently unrecognised
in children, who can continue to shed virus in their faeces for months after infection. In countries where
children are routinely vaccinated against hepatitis A, transmission primarily occurs between adults.[21] Foods
associated with outbreaks are typically eaten raw, and include fruits, vegetables, and shellfish.[21] The
disease may also be acquired by direct contact with contaminated water or ice (including shellfish harvested
from sewage-contaminated water), from contaminated frozen foods, or from foods contaminated by infected
food handlers.[22] [23]
5
Hepatitis A Theory
Pathophysiology
After oral inoculation the virus is transported across the intestinal epithelium by a poorly understood
transport mechanism. After travelling through the mesenteric veins to the liver, the virus enters hepatocytes,
THEORY
where replication of hepatitis A virus (HAV) occurs exclusively within the cytoplasm via RNA-dependent
polymerase. Virus particles are secreted into bile and blood from the infected hepatocytes. Viral particles are
excreted in stool or reabsorbed into the enterohepatic circulation.[19]
Liver injury occurs when cytotoxic T cells lyse the infected hepatocytes. Natural killer cells may also
contribute to cell lysis.[19] [24] [25]
An excessive host response (observable clinically by a marked degree of reduction of HAV RNA during acute
infection phase) is associated with severe hepatitis.[26]
Case history
Case history #1
A 34-year-old man presents 2 weeks after returning from a month-long trip to India. He denies attending
pre-travel vaccination clinic and did not take prophylaxis of any sort while in India. He reports a 6-day
history of malaise, anorexia, abdominal pain, nausea with emesis, and dark urine. He consumed salad
at a road-side vendor 3 weeks before onset of symptoms. On examination there is icterus. His alanine
transaminase (ALT) is 5660 units/L, and total bilirubin 153.9 micromols/L (9 mg/dL). Serum IgM anti-
hepatitis A virus antibodies are detected.
Other presentations
Hepatitis A can present atypically with severe thrombocytopenia.[3] Other atypical extrahepatic
manifestations of hepatitis A include vasculitis, arthritis, optic neuritis, transverse myelitis, aplastic
anaemia, and red cell aplasia.[4]
Hepatitis A Diagnosis
Approach
Post-exposure prophylaxis for both the patient and close contacts of the patient should not be delayed while
waiting for test results if reasonable clinical certainty exists about the probability of infection.
History
Thorough history can highlight relatively significant risk factors, including living in an endemic area, close
personal contact with an infected person, men who have sex with men, travel to high-risk areas, drug use,
known foodborne or waterborne outbreak, and homelessness.[21] In about one third of reported cases,
no risk factor is identified.[13]
History should also assess risk or history of other liver diseases such as hepatitis B and hepatitis C virus
infections and/or cirrhosis, as concomitant acute hepatitis A virus (HAV) infection in these circumstances
has a higher risk for progression to HAV acute liver failure.
Symptoms and signs

The incubation period averages 28 days (range 15-50 days).[1]
Most infections in children aged <6 years are asymptomatic; possible symptoms include fever, nausea,
anorexia, and malaise.[1] Only 10% of infected children develop jaundice.[33]
In adults and older children, clinical course can be divided into pre-icteric phase and icteric phase.[2]
The pre-icteric phase lasts 5-7 days characterised by abrupt onset of nausea, vomiting, abdominal pain,
fever, malaise, fatigue, and headache. Relatively less common symptoms include arthralgias, myalgias,
diarrhoea, constipation, cough, pruritus, and urticaria.[19]
Physical signs may include right upper quadrant pain with tender hepatomegaly, splenomegaly, posterior
cervical lymphadenopathy, evanescent rash, and bradycardia.[2] [19]
Within a few days to 1 week the icteric phase begins with dark urine, acholic stools, jaundice, and
DIAGNOSIS
pruritus.[2] With the onset of jaundice the pre-icteric phase symptoms usually diminish. Jaundice peaks
typically at 2 weeks.
Prolonged disease or acute liver failure
A minority of people (10% to 20%) have a prolonged or relapsing course. After initial infection, there is
a remission with partial or complete resolution of symptoms and abnormal liver tests. Relapse typically
occurs within 3 weeks and is milder than the initial infection. Immune-mediated manifestations (purpura,
arthralgia, nephritis) may occur.[34] A prolonged course can last several months with persistent fever,
pruritus, diarrhoea, jaundice, weight loss, and malabsorption.[19] [20]
Acute liver failure occurs in <1% of patients, and is characterised by worsening jaundice, coagulopathy,
and encephalopathy, due to severe impairment of hepatic functions, or severe necrosis of hepatocytes
in absence of pre-existing chronic liver disease.[35] [36] An excessive host immune response has been
implicated.[36] [37]
Diagnostic tests
Serum liver enzymes and bilirubin can be ordered as soon as clinical symptoms begin.[18] [19]
Transaminase levels may reach more than 10,000 units/L, although there is a little correlation between
7
level and disease severity. The serum alanine aminotransferase (ALT) is commonly higher than the serum
aspartate aminotransferase (AST). While alkaline phosphatase level is usually elevated minimally, the
bilirubin level is usually elevated to about 85.5 to 171.0 micromol/L (5-10 mg/dL).[38]
Blood urea, serum creatinine, and prothrombin time (PT) may also be measured at baseline. Acute
kidney injury has been reported in patients with HAV.[39] Patients with acute liver failure typically have a
prolonged PT.
Tests for immunoglobulin M (IgM) anti-HAV and IgG anti-HAV can be ordered concurrently. Serum IgM
anti-HAV antibodies are usually positive 5-10 days before onset of symptoms, peak during the acute or
early convalescent phase of the disease, and decline to undetectable levels over 6 months.[1] [20] [21]
Laboratory findings should be correlated with clinical features. Some asymptomatic patients may have
previous HAV infection with prolonged presence of IgM anti-HAV. False-positive laboratory results and
asymptomatic infection are both possible (more common in children aged younger than 6 years).[40] IgG
anti-HAV remains detectable for decades.
Reverse-transcriptase polymerase chain reaction to detect HAV RNA in stool, body fluids, serum, and
liver tissue is available. It is rarely necessary but may be considered to detect very early cases or if HAV-
IgM results are inconclusive.[1]
History and exam

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include living in an endemic area, close personal contact with an infected person, men
who have sex with men, travel to an endemic region, and exposure to a known foodborne outbreak.
fever (common)
DIAGNOSIS
• Often abrupt-onset and before the patient has jaundice.
malaise (common)
nausea and vomiting (common)

jaundice (common)
• Occurs in about 70% to 80% of symptomatic adult patients.[38] Typically peaks 2 weeks after infection.
Only 10% of infected children develop jaundice.[33]
DIAGNOSIS
Hepatitis A infection manifested here as jaundice of the conjunctivae and facial skin
CDC/ Dr. Thomas F. Sellers/Emory University; used with permission
hepatomegaly (common)
• Occurs in about 70% to 80% of symptomatic patients.[38] Often occurs with right upper quadrant pain.
right upper quadrant pain (common)

• Often occurs with tender hepatomegaly.
clay-coloured stools (common)

• Stools are acholic, giving rise to a clay colour.
Other diagnostic factors

fatigue (common)
9
headache (common)
dark urine (common)

• A feature of the icteric phase.
pruritus (common)
• A feature of the icteric phase.
arthralgias and myalgias (uncommon)

• Extrahepatic features may be evident.
cough (uncommon)
• Extrahepatic features may be evident.
diarrhoea (uncommon)
• May be a feature of the pre-icteric phase.
constipation (uncommon)
• May be a feature of the pre-icteric phase.
splenomegaly (uncommon)
• Possible physical sign on abdominal examination.
posterior cervical lymphadenopathy (uncommon)

• May be detected on examination.
evanescent rash (uncommon)

• Non-specific feature.
DIAGNOSIS
bradycardia (uncommon)
• May be detected on examination.
Risk factors
Strong
living in endemic region
• In developing countries with poor sanitation >90% of children are infected before 10 years of age.[10]
travel to endemic region

• Unvaccinated people from developed countries who travel to areas of high or intermediate hepatitis A
endemicity have a significant risk for acquiring hepatitis A.[21]
• Risk is highest for people who live in or visit rural areas, frequently eat and drink in places with poor
sanitation, or trek in backcountry areas.[21]
close personal contact with an infected person
• Risk factor for infection.[13] Hepatitis A virus infection risk is increased in household contacts of
international adoptees.[21]
men who have sex with men

• Risk factor for infection.[13] Outbreaks of hepatitis A in men who have sex with men have been
reported frequently in the US and Europe.[21]
known foodborne outbreak

• Foods associated with outbreaks are typically eaten raw, and include fruits, vegetables, and
shellfish.[21] The disease may also be acquired by direct contact with contaminated water or ice
(including shellfish harvested from sewage-contaminated water), from contaminated frozen foods, or
from foods contaminated by infected food handlers.[22][23]
illegal drug use

• The number of cases of hepatitis A virus infection associated with injection drug use in the US has
increased rapidly since 2015. Injection drug use is the most commonly reported risk factor in the
US.[13]
homelessness
• The number of cases of hepatitis A virus infection associated with homelessness in the US has
increased rapidly since 2015.[13]
Weak
occupational exposure
• People who work in research laboratories handling hepatitis A-infected material, and people who
work with non-human primates, are at risk of occupational infection. Healthcare workers and workers
exposed to sewage are not at significantly increased risk.[21]
DIAGNOSIS
11
Investigations
1st test to order
Test Result
serum transaminases elevated
• Test should be ordered as soon as clinical symptoms begin.[18] [19]
Transaminase levels may reach more than 10,000 units/L, although
there is little correlation between level and disease severity. The
serum alanine aminotransferase is commonly higher than the serum
aspartate aminotransferase. The serum transaminases elevation
usually precedes bilirubin elevation. Alkaline phosphatase level is
usually elevated minimally.
serum bilirubin elevated
• The bilirubin level is usually elevated to about 85.5 to 171.0 micromol/
L (5-10 mg/dL).[38]
blood urea elevated in acute liver
injury/failure
• Acute kidney injury has been reported in patients with HAV.[39] This,
with other markers, may also be indicative of acute liver failure.
serum creatinine elevated above 177
micromol/L (2 mg/dL) in
• Acute kidney injury has been reported in patients with HAV.[39] This,
acute liver injury/failure
with other markers, may also be indicative of acute liver failure.
prothrombin time may be mildly
prolonged; more marked
• Mainly ordered as baseline test.
• Mild elevations of about 11-26 seconds are common in HAV infection. prolongation with acute
liver failure
IgM anti-hepatitis A virus (HAV) positive

• High sensitivity and specificity when used on specimens from
persons with typical symptoms.[18] Usually can be detected 5-10
DIAGNOSIS
days before symptom onset; levels become undetectable by 6 months

after symptom onset.[1] [20] [21] Can be ordered along with IgG anti-
HAV.
Other tests to consider
Test Result
IgG anti-hepatitis A virus (HAV) positive
• Levels begin to rise soon after IgM levels and stay elevated
throughout the person's lifetime; therefore, positive result can mean
prior infection or recent disease and should be interpreted along with
results of IgM anti-HAV and clinical features.[1] [20] Can be ordered
along with IgM anti-HAV.
hepatitis A virus RNA detection nucleic acid amplification
techniques using body
• High sensitivity and specificity, but very rarely used in routine
fluids serum, stool, and
settings.
liver tissue
• May be used to detect very early cases or if serology is
inconclusive.[1]
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Acute hepatitis B • Clinical features of viral • Anti-hepatitis A virus IgM is
hepatitis in a person with negative, whereas hepatitis
a history of injection drug B surface antigen and/or IgM
use, nasal snorting of drugs, antibody to hepatitis B core
multiple sexual partners, antigen are positive.
or transfusion of blood
products before donors were
routinely screened. Disease
incubation period is longer.
Hepatitis E • Clinical features of viral • Test for anti-hepatitis E virus

hepatitis in a person with IgM in acute-phase sera.
a history of recent travel to
endemic areas or exposure
to an infected person
or contaminated water.
Hepatitis E is often more
severe in pregnant women.
Acute hepatitis C • Clinical features of viral • Anti-hepatitis C virus (HCV)

hepatitis in men who have positive by enzyme-linked
sex with men, or in people immunosorbent assay
with a history of injection (ELISA) and confirmed by
drug use, positive HIV recombinant immunoblot
status, an occupational assay (RIBA) or positive
exposure in the previous 6 HCV RNA.
months, or blood transfusion • Anti-HCV may be negative
before donors were routinely in acute HCV infection;
screened. thus, patient is tested for
HCV RNA if anti-HCV is
DIAGNOSIS
negative, the patient has
HCV-associated risk factors,
and acute HCV infection is
suspected.
Epstein-Barr virus (EBV) • Clinical features of viral • Negative serology results

infection hepatitis with no history for all types of viral hepatitis.
of exposure to other Atypical lymphocytes tend
organisms that can cause to be present. EBV IgM and
hepatitis; classically display IgG positive.
lymphadenopathy and
splenomegaly in EBV
infection.
Coxsackie virus • Classically displays buccal • Hand-foot-and-mouth

or pharyngeal lesions with disease mainly is a clinical
Coxsackie virus infection. diagnosis. Coxsackie
serology can be helpful
if available. Atypical
lymphocytes tend to be
present.
13

symptoms
Cytomegalovirus (CMV) • Clinical features of viral • Negative serology results
infection hepatitis with no history of for all types of viral hepatitis.
exposure to other organisms Atypical lymphocytes tend
that can cause hepatitis. to be present. CMV IgM
and IgG positive. CMV
polymerase chain reaction in
blood positive.
Herpes simplex virus • Clinical features of viral • Negative serology results

infection hepatitis with no history of for all types of viral hepatitis.
exposure to other organisms Mainly a clinical diagnosis
that can cause hepatitis; (aided by presence of typical
may display characteristic muco-cutaneous lesions).
cutaneous ulceration. A liver biopsy confirms
diagnosis.
Auto-immune hepatitis • Approximately 90% of cases • Erythrocyte sedimentation

occur in women. Other auto- rate elevated.
immune disorders may be • Serum electrophoresis
present; 25% to 40% of and serum autoantibodies:
cases can present with acute patients may have
hepatitis. Hepatitis A virus serum gamma-globulin
(HAV) has been described concentrations more
as a possible trigger for auto- than twice normal, and
immune hepatitis.[41] [42] sometimes antinuclear
antibodies and/or anti-
smooth muscle (anti-actin)
antibodies. Patients with
another subtype may have
normal or only slightly
elevated serum gamma-
globulin concentrations but
will have antibodies against
DIAGNOSIS
a particular cytochrome
p450 isoenzyme that are
called anti-LKM (liver kidney
microsome).
• Liver biopsy is characterised
by a periportal lesion or
interface hepatitis (a portal
mononuclear and plasma
cell infiltrate).
Alpha-1 antitrypsin • Uncommonly presents as • Alpha-1 antitrypsin serum

disease acute hepatitis. level reduced; phenotyping
demonstrating characteristic
alpha-1 antitrypsin-variant
proteins. Liver biopsy stain
for periodic acid-Schiff-
positive inclusions.
Alcoholic hepatitis • History of excessive alcohol • AST/ALT ratio of at least

consumption. 2:1 in up to 80% of cases.
• Hepatomegaly and jaundice Full blood count may show
are found in approximately

symptoms
95% and 55% of persons anaemia, leukocytosis, and/
presenting with alcoholic or thrombocytopenia.
hepatitis, respectively.
Ischaemic hepatitis • Also referred to as 'shock • Negative viral hepatitis

liver'. History of injury or serologies.
hypotension, postoperative
patient.
Drug-induced hepatitis • History of excessive • History of drug consumption;

paracetamol ingestion or improvement usually occurs
therapeutic amounts of with discontinuation.
paracetamol in a patient
with alcoholic liver disease
or alcohol ingestion; other
therapeutic drugs may
cause hepatitis (e.g.,
isoniazid, non-steroidal anti-
inflammatory drugs, beta-
lactam antibiotics, sulfa-
containing compounds,
insulin-sensitising drugs);
may affect men and women
of all ages but more common
in women and the elderly.
Wilson's disease • Rarely presents after • 24-hour urine for copper

age 40 years without >100 micrograms, and
neuropsychiatric symptoms; serum ceruloplasmin <180
rarely presents as acute mg/L (18 mg/dL) is positive
hepatitis. for Wilson's disease. Liver
• Kayser-Fleischer rings upon biopsy and assay of copper
slit-lamp ophthalmological >250 micrograms/g dry
examination. weight indicates Wilson's
DIAGNOSIS
disease. A liver copper level
of <150 micrograms/g dry
weight rules out Wilson's
disease.
Eye demonstrating
Kayser-Fleischer ring
Adapted from Aggarwal
A, Bhatt M. BMJ 2009;
339:b3494; copyright
2009 by the BMJ
Publishing Group
15
Hepatitis A Management
Approach
Management strategies are individualised and should involve consultants when appropriate, depending on
specific patient characteristics.
Post-exposure prophylaxis
Active or passive immunisation is available for protection following exposure to hepatitis A virus (HAV)
infection. Recommendations concerning post-exposure prophylaxis may differ geographically, so specific
national guidelines should be consulted.[21] [31] [32] [43][44]
For immunocompetent people (aged ≥12 months)
For healthy people with recent HAV exposure (<2 weeks) who have not completed the two-dose hepatitis
A vaccine series, the the Centers for Disease Control and Prevention (CDC) recommends:[21]
• A single dose of hepatitis A vaccine as soon as possible

• Discretionary co-administration of immunoglobulin for people aged >40 years (depending on
provider assessment of individual risk factors for HAV infection and/or HAV-related complications).
Immunocompromised people or those with chronic liver disease (aged ≥12 months)
For immunocompromised people or those with chronic liver disease who have not completed the two-
dose hepatitis A vaccine series, the CDC recommends:[21]
• Immunoglobulin and a single dose of hepatitis A vaccine simultaneously at anatomically discrete

sites, as soon as possible (<2 weeks).
Infants aged <12 months/vaccine contraindicated
Children younger than 12 months and those with a history of life-threatening allergy following
administration of hepatitis A vaccine (or severe allergy to any component of the vaccine) should
receive:[21] [CDC: hepatitis A FAQs for health professionals] (http://www.cdc.gov/hepatitis/HAV/
HAVfaq.htm)
• Immunoglobulin as soon as possible (<2 weeks since exposure)

Patients who require post-exposure prophylaxis.
The CDC recommends post-exposure prophylaxis for the following patient populations: [CDC: hepatitis A
FAQs for health professionals] (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
• All previously unvaccinated people exposed to (or at risk of exposure to) people with serologically
confirmed hepatitis A, including:
• Household members
• Sexual contacts
MANAGEMENT
• People who have shared injection drugs with someone with hepatitis A
• Carers not using personal protective equipment
• All previously unvaccinated members of staff and attendees at childcare centres where:
• One or more cases of hepatitis A infection is recognised in children or employees
• Cases are recognised in two or more households of centre attendees
• Food handlers in the same establishment of another food handler who receives a diagnosis of
hepatitis A
• People who have close contact with infected patients, if an epidemiological investigation indicates
hepatitis A transmission has occurred:
• In a school
• Among hospital patients
• Between patients and hospital staff.
Further specific considerations are provided online by the CDC. [CDC: hepatitis A FAQs for health
professionals] (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
Confirmed infection: supportive care

Treatment for HAV infection is primarily supportive, including appropriate rest when necessary.[19]
Excessive paracetamol and alcohol should be avoided.[2] [18] There are no specific antiviral therapies
available.
Once acute infection occurs, management is largely outpatient-based. Rarely, hospitalisation may
become necessary for volume depletion, coagulopathy, or encephalopathy.[18]
Contact precautions are taken during the infectious period, particularly in the incontinent patient group
or patients requiring nappies. The infectious period lasts for about 2 weeks after the onset of illness in
healthy individuals. Certain patient groups remain infectious for up to 6 months. This includes children
and immunocompromised patients.[2]
Confirmed infection: referral for liver transplant

In <1% of patients, acute liver failure occurs, characterised by worsening jaundice, coagulopathy, and
encephalopathy.[35] [36] Prompt referral to centres experienced in liver transplantation is warranted
in such cases. This is of particular significance in patients with coexisting hepatitis C or hepatitis
B virus infections, or cirrhosis of any cause. HAV infection in these conditions has a higher risk for
acute liver failure. A prognostic index consisting of four clinical and laboratory features (serum alanine
aminotransferase (ALT) <2600 units/L, creatinine >177 micromoles/L [>2 mg/dL], intubation, pressors)
predicts the likelihood of transplantation/death significantly better than other published models.[35] The
lower ALT levels that were found to be one of the indicators of poor prognosis were thought to be due to
extensive necrosis at presentation.[35] MANAGEMENT
17
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Initial ( summary )
unvaccinated people with recent
exposure to hepatitis A (<2 weeks)
1st hepatitis A vaccine and/or

immunoglobulin
Acute ( summary )
confirmed hepatitis A
1st supportive care
with acute liver failure plus liver transplant

MANAGEMENT
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Initial
unvaccinated people with recent
exposure to hepatitis A (<2 weeks)
1st hepatitis A vaccine and/or

immunoglobulin
Primary options
» hepatitis A vaccine: administer according to

current recommended schedule
-and/or-
» normal immunoglobulin human: consult
specialist for guidance on intramuscular dose
» Active or passive immunisation is available for

protection following exposure to hepatitis A virus
(HAV) infection.
» The Centers for Disease Control and

Prevention (CDC) recommends a single dose
of hepatitis A vaccine as soon as possible post-
exposure (<2 weeks) for immunocompetent
people (aged ≥12 months) who have not
completed the two-dose hepatitis A vaccine
series:[21] [CDC: hepatitis A FAQs for health
professionals] (http://www.cdc.gov/hepatitis/
HAV/HAVfaq.htm) Co-administration of
immunolobulin (at a discrete anatomical site)
may be considered for people aged >40
years with risk factors for HAV infection or its
complications.
» For immunocompromised people, or those with

chronic liver disease, who have not completed
the two-dose hepatitis A vaccine series, the
CDC recommends immunoglobulin and a single
dose of hepatitis A vaccine simultaneously (at
a discrete anatomical site), as soon as possible
(<2 weeks since exposure).
» Infants aged <12 months and those with

a history of life-threatening allergy following
administration of hepatitis A vaccine (or severe
allergy to any component of the vaccine)
should receive immunoglobulin as soon as
possible (<2 weeks since exposure).[21] [CDC:
MANAGEMENT
hepatitis A FAQs for health professionals] (http://

www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
» Recommendations concerning post-exposure

prophylaxis may differ geographically, so specific
19
Initial
national guidelines should be consulted.[21] [31]
[32] [43][44]
» Intramuscular immunoglobulin may need to be

obtained from a specialist centre; it is not widely
commercially available.
Acute
confirmed hepatitis A
confirmed hepatitis A 1st supportive care
» Treatment for infection is primarily supportive,

including appropriate rest when necessary.[19]
No specific antiviral therapy is available.
» Excess paracetamol and alcohol should be

avoided.[2] [18]
» Rarely, hospitalisation may become

necessary for volume depletion, coagulopathy,
encephalopathy, or severe prostration.[18] This
is particularly important in patients with co-
infection with hepatitis B virus, hepatitis C virus,
or cirrhosis of any cause, as acute hepatitis A
virus (HAV) infection in these conditions has a
higher risk for severe disease.
with acute liver failure plus liver transplant
Treatment recommended for ALL patients in
selected patient group
» In <1% of patients, acute liver failure
occurs characterised by worsening jaundice,
coagulopathy, and encephalopathy.[35] [36]
Prompt referral to centres experienced in liver
transplantation is warranted in such cases.
This is of particular significance in patients
with coexisting hepatitis C or hepatitis B virus
infections, or cirrhosis of any cause. Hepatitis A
virus (HAV) infection in these conditions has a
higher risk for acute liver failure.
» A prognostic index consisting of four clinical

and laboratory features (serum alanine
aminotransferase [ALT] <2600 units/L,
creatinine >177 micromoles/L [>2 mg/dL],
intubation, pressors) predicts the likelihood of
transplantation/death significantly better than
other published models.[35] The lower ALT
levels that were found to be one of the indicators
MANAGEMENT
of poor prognosis were thought to be due to

extensive necrosis at presentation.[35]
Primary prevention
The major mechanism of spread is through oral inoculation of faecally excreted virus, which makes this
infection preventable through simple public health measures. The virus may survive for up to 4 hours on the
fingertips; adherence to strict handwashing after handling faecal material is of utmost importance.[27]
In the US, routine hepatitis A vaccination is recommended for:[21] [28] [29] [30]
Children and adolescents:
• All children aged 12-23 months

• Children and adolescents aged 2-18 years who have not previously received the hepatitis A
vaccination (i.e., children and adolescents are recommended for catch up vaccination).
People (including pregnant women) at increased risk of hepatitis A virus (HAV) infection:
• International travellers
• Men who have sex with men
• People who use injection or noninjection drugs (i.e., those who use illegal drugs)
• People with occupational risk of exposure
• People who anticipate close personal contact with an international adoptee
• People experiencing homelessness
• People with HIV infection aged ≥1 year.
People (including pregnant women) at risk of developing serious complications from HAV infection:
• People with chronic liver disease

• People with HIV infection.
The Advisory Committee on Immunization Practices (ACIP) also recommends hepatitis A vaccination for:[21]
• Unvaccinated people in outbreak settings who are at risk for HAV infection or at risk for severe disease
from HAV
• People in settings that provide services to adults in which a high proportion of those persons have risk
factors for HAV infection
• Any people who request vaccination.
Refer to ACIP vaccine recommendations and guidelines for further details. [CDC: ACIP vaccine
recommendations and guidelines] (https://www.cdc.gov/vaccines/hcp/acip-recs)
Hepatitis A vaccine recommendations may differ in other countries.[31] [32]
Secondary prevention
Active or passive immunisation is available for protection following exposure to hepatitis A virus (HAV)
infection. Recommendations concerning post-exposure prophylaxis may differ geographically, so specific
national guidelines should be consulted.[21][31] [32] [43][44]
Immunocompetent people (aged ≥12 months)

MANAGEMENT
For healthy people with recent HAV exposure (<2 weeks) who have not completed the two-dose hepatitis A
vaccine series, the US Centers for Disease Control and Prevention (CDC) recommends:[21]
• A single dose of the hepatitis A vaccine as soon as possible
21
• Discretionary co-administration of immunoglobulin for people aged >40 years (depending on provider
assessment of individual risk factors for HAV infection and/or HAV-related complications).
Immunocompromised people or chronic liver disease (aged ≥12 months)
For immunocompromised people or those with chronic liver disease who have not completed the two-dose
hepatitis A vaccine series, the CDC recommends:[21]
• Immunoglobulin and a single dose of hepatitis A vaccine simultaneously at anatomically discrete sites,
as soon as possible (<2 weeks).
Infants aged <12 months/vaccine contraindicated
Children younger than 12 months and those with a history of a life-threatening allergy following
administration of hepatitis A vaccine (or severe allergy to any component of the vaccine) should receive:[21]
[CDC: hepatitis A FAQs for health professionals] (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
• Immunoglobulin as soon as possible (<2 weeks since exposure).
Patients who require post-exposure prophylaxis
The CDC recommends post-exposure prophylaxis for the following patient populations: [CDC: hepatitis A
FAQs for health professionals] (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
• All previously unvaccinated people exposed to (or at risk of exposure to) people with serologically
confirmed hepatitis A including:
• Household members
• Sexual contacts
• People who have shared injection drugs with someone with hepatitis A
• Carers not using personal protective equipment
• All previously unvaccinated members of staff and attendees at childcare centres where:
• One or more cases of hepatitis A infection is recognised in children or employees

• Cases are recognised in two or more households of centre attendees
• Food handlers in the same establishment of another food handler who receives a diagnosis of
hepatitis A
• People who have close contact with infected patients, if an epidemiological investigation indicates
hepatitis A transmission has occurred:
• In a school
• Among hospital patients
• Between patients and hospital staff.
Further specific considerations are provided online by the CDC. [CDC: hepatitis A FAQs for health
professionals] (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)
MANAGEMENT
Patient discussions
Physicians should advise patients to wash their hands thoroughly after nappy changing and defecation,
and disposal of sanitary wastes. Careful food-handling practices, particularly of fresh produce and
shellfish, are of utmost importance. Patients at high risk for acquiring hepatitis A virus (HAV) infection
should be advised about immunisation: for example, travellers to certain countries, injection drug users,
men who have sex with men, persons receiving clotting factor concentrates, and individuals with chronic
liver disease. Patients should avoid excessive paracetamol and alcohol intake.[2] [18] Children should not
return to school or day care until at least 1 week after onset of the illness.[1]
MANAGEMENT
23
Hepatitis A Follow up
Monitoring
Monitoring
FOLLOW UP
Patents are followed up with weekly measurements of serum alanine aminotransferase, aspartate
aminotransferase, and gamma-GT until confirmation of resolution of transaminitis.
Complications
Complications Timeframe Likelihood
FOLLOW UP
acalculous cholecystitis variable low
Related to differential host immune response. Patients require supportive care and referral to a
gastrointestinal consultant.
pancreatitis variable low
Patents require referral to a gastrointestinal specialist.
aplastic anaemia variable low
Patents require referral to a haematology specialist.
auto-immune haemolysis variable low
haematology consultant.
auto-immune thrombocytopenic purpura variable low
haemolysis (G6PD deficiency) variable low
Guillain-Barre syndrome variable low
Patients often require corticosteroid administration and referral to a neurology consultant.
mononeuritis multiplex variable low
post-viral encephalitis variable low
transverse myelitis variable low
25
Complications Timeframe Likelihood

acute kidney injury variable low
FOLLOW UP
Rare in hepatitis A virus (HAV) infection.[39] The exact process remains to be elucidated, but usually
occurs within the first 10 days of the appearance of jaundice.
Although some cases may be due to pre-renal azotaemia, biopsies in other cases have indicated other
mechanisms of damage, including interstitial nephritis, mesangial proliferative glomerulonephritis, or
nephritic syndrome.
Most cases require haemodialysis and some may warrant plasmapheresis.
cutaneous vasculitis variable low
Related to differential host immune response. Skin biopsy may be required.
cryoglobulinaemia variable low
Serum cryoglobulin levels are diagnostic. Patients should be transferred to a tertiary centre for evaluation.
reactive arthritis variable low
Patients may require transfer to a tertiary centre for evaluation.
Prognosis
Approximately 85% of individuals infected with hepatitis A virus (HAV) have full clinical and biochemical
recovery within a 3-month period with nearly all individuals recovering within 6 months.[45] In about 10%
to 20% of symptomatic patients, a prolonged and relapsing course can occur lasting several months with
persistent fever, pruritus, diarrhoea, jaundice, weight loss, and malabsorption.[19] [20]
Death from hepatitis A is rare. In 2021, US case fatality rates were unreliable for ages 0-44 years, 0.06 per
100,000 people for ages 45-64 years, and 0.13 per 100,000 people for ages ≥65 years.[13]
In <1% of patients, acute liver failure occurs characterized by worsening jaundice, coagulopathy, and
encephalopathy.[35] [36] These patients require immediate referral for liver transplant assessment. The 1-
year survival rate for patients who receive liver transplantation for acute HAV infection is 69%.[46]
Hepatitis A Guidelines
Diagnostic guidelines
Europe
Immunisation guidelines for Ireland: hepatitis A (ht tps://www.hse.ie/eng/

health/immunisation/hcpinfo/guidelines/immunisationguidelines.html)
Published by: Royal College of Physicians of Ireland Last published: 2022
North America
Recommended immunization schedule for adults aged 19 years or older

(ht tps://www.cdc.gov/vaccines/schedules/index.html)
Published by: Centers for Disease Control and Prevention Last published: 2023
Recommended immunization schedule for children and adolescents aged 18
GUIDELINES
years or younger (ht tps://www.cdc.gov/vaccines/schedules/index.html)
Viral hepatitis testing (ht tps://www2.gov.bc.ca/gov/content/health/

practitioner-professional-resources/bc-guidelines/guidelines-by-
alphabetical-listing)
Published by: Guidelines and Protocols Advisory Committee (British Last published: 2021
Columbia)
Prevention of hepatitis A virus infection in the US (ht tps://www.cdc.gov/

mmwr/volumes/69/rr/rr6905a1.htm)
Serological testing for suspected viral hepatitis (ht tps://

act t.albertadoctors.org/CPGs)
Published by: Alberta Medical Association Last published: 2006
(reviewed in 2014)
Oceania
Hepatitis A – national guidelines for public health units (ht tps://

www.health.gov.au/resources/publications/hepatitis-a-cdna-national-
guidelines-for-public-health-units)
Published by: Communicable Diseases Network Australia Last published: 2023
Hepatitis A control guideline (ht tps://www.health.nsw.gov.au/Infectious/

controlguideline/Pages/default.aspx)
Published by: Government of New South Wales Last published: 2019
27
Treatment guidelines
United Kingdom
Immunisation against infectious disease: the green book - hepatitis A (ht tps://
www.gov.uk/government/collections/immunisation-against-infectious-
disease-the-green-book)
Published by: UK Health Security Agency Last published: 2022
Public health control and management of hepatitis A (ht tps://www.gov.uk/

government/publications/hepatitis-a-infection-prevention-and-control-
guidance)
Published by: Public Health England Last published: 2017
Europe
GUIDELINES
Immunisation guidelines for Ireland: hepatitis A (ht tps://www.hse.ie/eng/

health/immunisation/hcpinfo/guidelines/immunisationguidelines.html)
Published by: Royal College of Physicians of Ireland Last published: 2022
Hepatitis A and B vaccination of drug users in primary care and criteria for
audit (ht tps://www.drugsandalcohol.ie/13636)
Published by: Royal College of General Practitioners Last published: 2004
International
Foodborne disease outbreaks: guidelines for investigation and control

(ht tps://apps.who.int/iris/handle/10665/43771)
Published by: World Health Organization Last published: 2008
North America
Recommended immunization schedule for adults aged 19 years or older

(t tps://www.cdc.gov/vaccines/schedules/index.html)
Recommended immunization schedule for children and adolescents aged 18

years or younger (t tps://www.cdc.gov/vaccines/schedules/index.html)
Sexually transmit ted diseases treatment guidelines (ht tps://www.cdc.gov/std/

treatment)
Prevention of hepatitis A virus infection in the US (ht tps://www.cdc.gov/

mmwr/volumes/69/rr/rr6905a1.htm)
GUIDELINES
Advisory: screening and treatment of viral hepatitis in people with substance

use disorders (ht tps://store.samhsa.gov)
Published by: Substance Abuse and Mental Health Services Last published: 2021
Administration
Oceania
Hepatitis A – national guidelines for public health units (ht tps://

www.health.gov.au/resources/publications/hepatitis-a-cdna-national-
guidelines-for-public-health-units)
Published by: Communicable Diseases Network Australia Last published: 2023
Hepatitis A control guideline (ht tps://www.health.nsw.gov.au/Infectious/

controlguideline/Pages/default.aspx)
Published by: Government of New South Wales Last published: 2019
29
Hepatitis A Online resources
Online resources
1. CDC: ACIP vaccine recommendations and guidelines (https://www.cdc.gov/vaccines/hcp/acip-recs)
(external link)
2. CDC: hepatitis A FAQs for health professionals (http://www.cdc.gov/hepatitis/HAV/HAVfaq.htm)

(external link)
ONLINE RESOURCES
Hepatitis A References
Key articles
• Committee on Infectious Diseases, American Academy of Pediatrics; Kimberlin D, Barnett E, Lynfield
REFERENCES
R, et al. Hepatitis A. In: Red Book: 2021–2024 report of the Committee on Infectious Diseases. 32nd
ed. Elk Grove Village, IL: American Academy of Pediatrics; 2021.
• Kemmer NM, Miskovsky EP. Hepatitis A. Infect Dis Clin North Am. 2000 Sep;14(3):605-15. Abstract
(http://www.ncbi.nlm.nih.gov/pubmed/10987112?tool=bestpractice.bmj.com)
• Nelson NP, Weng MK, Hofmeister MG, et al. Prevention of hepatitis A virus infection in the
United States: recommendations of the Advisory Committee on Immunization Practices, 2020.
MMWR Recomm Rep. 2020 Jul 3;69(5):1-38. Full text (https://www.cdc.gov/mmwr/volumes/69/rr/
rr6905a1.htm) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/32614811?tool=bestpractice.bmj.com)
References
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R, et al. Hepatitis A. In: Red Book: 2021–2024 report of the Committee on Infectious Diseases. 32nd
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2. Brundage SC, Fitzpatrick AN. Hepatitis A. Am Fam Physician. 2006 Jun 15;73(12):2162-8.
Full text (http://www.aafp.org/afp/20060615/2162.html) Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/16848078?tool=bestpractice.bmj.com)
3. Shenoy R, Nair S, Kamath N. Thrombocytopenia in hepatitis A: an atypical presentation. J

Trop Pediatr. 2004 Aug;50(4):241-2. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/15357567?
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4. Schiff ER. Atypical clinical manifestations of hepatitis A. Vaccine. 1992;10(suppl 1):S18-S20. Abstract
5. Abutaleb A, Kottilil S. Hepatitis A: epidemiology, natural history, unusual clinical manifestations,

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6. Hodges M, Sanders E, Aitken C. Seroprevalence of hepatitis markers; HAV, HBV, HCV and HEV
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16. Feinstone SM, Kapikian AZ, Purceli RH. Hepatitis A: detection by immune electron microscopy of
a viruslike antigen associated with acute illness. Science. 1973 Dec 7;182(4116):1026-8. Abstract
17. Coulepis AG, Locarnini SA, Westaway EG, et al. Biophysical and biochemical characterization
of hepatitis A virus. Intervirology. 1982;18(3):107-27. Abstract (http://www.ncbi.nlm.nih.gov/
18. Kemmer NM, Miskovsky EP. Hepatitis A. Infect Dis Clin North Am. 2000 Sep;14(3):605-15. Abstract
19. Cuthbert JA. Hepatitis A: old and new. Clin Microbiol Rev. 2001 Jan;14(1):38-58. Full text
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88961) Abstract (http://www.ncbi.nlm.nih.gov/
20. Centers for Disease Control and Prevention. Epidemiology and prevention of vaccine-preventable
diseases. 14th ed. Atlanta, GA: Centers for Disease Control and Prevention; 2021. Full text (https://
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21. Nelson NP, Weng MK, Hofmeister MG, et al. Prevention of hepatitis A virus infection in the
United States: recommendations of the Advisory Committee on Immunization Practices, 2020.
MMWR Recomm Rep. 2020 Jul 3;69(5):1-38. Full text (https://www.cdc.gov/mmwr/volumes/69/rr/
rr6905a1.htm) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/32614811?tool=bestpractice.bmj.com)
22. Centers for Disease Control and Prevention. Viral hepatitis: multistate outbreak of hepatitis A virus
infections linked to frozen organic strawberries. Sep 2023 [internet publication]. Full text (https://
www.cdc.gov/hepatitis/outbreaks/2023/hav-contaminated-food/index.htm)
23. Centers for Disease Control and Prevention. Morbidity and mortality weekly report: widespread
community transmission of hepatitis A virus following an outbreak at a local restaurant - Virginia,
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33. World Health Organization. Hepatitis A. July 2023 [internet publication]. Full text (https://www.who.int/
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34. Glikson M, Galun E, Oren R, et al. Relapsing hepatitis A: review of 14 cases and literature survey.
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46. Jung DH, Hwang S, Lim YS, et al. Outcome comparison of liver transplantation for hepatitis A-related
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35
Hepatitis A Images
Images
IMAGES
Figure 1: Geographical distribution of the prevalence of hepatitis A (based on summary of available data)
CDC website; used with permission
Hepatitis A Images
IMAGES
Figure 2: An electron micrograph of the hepatitis A virus
CDC/Betty Partin; used with permission
37
IMAGES Hepatitis A Images
Figure 3: Hepatitis A infection manifested here as jaundice of the conjunctivae and facial skin
CDC/ Dr. Thomas F. Sellers/Emory University; used with permission
Hepatitis A Images
IMAGES
Figure 4: Eye demonstrating Kayser-Fleischer ring
Adapted from Aggarwal A, Bhatt M. BMJ 2009; 339:b3494; copyright 2009 by the BMJ Publishing Group
39
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Contributors:
// Authors:
Doan Y Dao, MD
Assistant Professor of Medicine
Director, Center of Excellence for Liver Disease in Vietnam, Johns Hopkins School of Medicine, Department
of Medicine, Division of GI and Hepatology, Baltimore, MD
DISCLOSURES: DYD receives grants from Roche, serves as guest director of hepatology for Tech
University, and is a member of the Data and Safety Monitoring Board of the IQVIA.
// Acknowledgements:
Dr Doan Dao would like to gratefully acknowledge Dr Musaddiq Waheed and the late Dr Fida A. Khan, the
previous contributors to this topic.
DISCLOSURES: MW and FAK declared that they have no competing interests.
// Peer Reviewers:
Howard J. Worman, MD
Professor of Medicine and Cell Biology
Columbia University College of Physicians and Surgeons, New York, NY
DISCLOSURES: HJW declares that he has no competing interests.
Srikrishna Nagri, MD
Gastroenterologist
Dartmouth-Hitchcock Nashua, Nashua, NH
DISCLOSURES: SN declares that he has no competing interests.
George Y. Wu, MD, PhD

Professor of Medicine
University of Connecticut Health Center, Farmington, CT
DISCLOSURES: GYW is on the medical advisory boards of the following: Gilead Sciences, Bristol-Myers
Squibb, AbbVie, and Intercept.
Kit tichai Promrat, MD

Assistant Professor
Division of Gastroenterology, Department of Medicine, Brown University, RI
DISCLOSURES: KP declares that he has no competing interests.
Pierre Van Damme, MD, PhD

Professor
Director of Vaccine & Infectious Disease Institute, University of Antwerp, Antwerp, Belgium
DISCLOSURES: PVD has been and still is principal investigator of vaccine trials for several vaccine
manufacturing companies, from which the university obtained and obtains research contracts and funds for
conducting such vaccine trials.

Hepatitis A

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Hepatitis A

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Hepatitis A

Straight to the point of care

Last updated: Feb 21, 2024

Immunoglobulin M anti-hepatitis A virus serology is the test of choice for diagnosis.

No specific therapy is available, and treatment is usually supportive.

Geographical distribution of the prevalence of hepatitis A (based on summary of available data)

Symptoms and signs

Prolonged disease or acute liver failure

History and exam

• Often abrupt-onset and before the patient has jaundice.

nausea and vomiting (common)

right upper quadrant pain (common)

clay-coloured stools (common)

Other diagnostic factors

dark urine (common)

arthralgias and myalgias (uncommon)

posterior cervical lymphadenopathy (uncommon)

evanescent rash (uncommon)

travel to endemic region

men who have sex with men

known foodborne outbreak

illegal drug use

IgM anti-hepatitis A virus (HAV) positive

days before symptom onset; levels become undetectable by 6 months

Other tests to consider

Condition Differentiating signs / Differentiating tests

Hepatitis E • Clinical features of viral • Test for anti-hepatitis E virus

Acute hepatitis C • Clinical features of viral • Anti-hepatitis C virus (HCV)

Epstein-Barr virus (EBV) • Clinical features of viral • Negative serology results

Coxsackie virus • Classically displays buccal • Hand-foot-and-mouth

Condition Differentiating signs / Differentiating tests

Herpes simplex virus • Clinical features of viral • Negative serology results

Auto-immune hepatitis • Approximately 90% of cases • Erythrocyte sedimentation

Alpha-1 antitrypsin • Uncommonly presents as • Alpha-1 antitrypsin serum

Alcoholic hepatitis • History of excessive alcohol • AST/ALT ratio of at least

Condition Differentiating signs / Differentiating tests

Ischaemic hepatitis • Also referred to as 'shock • Negative viral hepatitis

Drug-induced hepatitis • History of excessive • History of drug consumption;

Wilson's disease • Rarely presents after • 24-hour urine for copper

For immunocompetent people (aged ≥12 months)

• A single dose of hepatitis A vaccine as soon as possible

• Immunoglobulin and a single dose of hepatitis A vaccine simultaneously at anatomically discrete

• Immunoglobulin as soon as possible (<2 weeks since exposure)

• One or more cases of hepatitis A infection is recognised in children or employees

Confirmed infection: supportive care

Confirmed infection: referral for liver transplant

Treatment algorithm overview

1st hepatitis A vaccine and/or

1st supportive care

with acute liver failure plus liver transplant

1st hepatitis A vaccine and/or

» hepatitis A vaccine: administer according to

» Active or passive immunisation is available for

» The Centers for Disease Control and

» For immunocompromised people, or those with

» Infants aged <12 months and those with

hepatitis A FAQs for health professionals] (http://

» Recommendations concerning post-exposure

» Intramuscular immunoglobulin may need to be

confirmed hepatitis A 1st supportive care

» Treatment for infection is primarily supportive,

» Excess paracetamol and alcohol should be

» Rarely, hospitalisation may become

» A prognostic index consisting of four clinical