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Hepatitis A is a common cause of acute hepatitis spread through the fecal-oral route. This case report describes a 30-year-old male who presented with jaundice and flu-like symptoms and was found to have hepatitis A infection based on laboratory testing showing significant liver inflammation. While hepatitis A generally causes a self-limited illness, this case illustrates the importance of considering the diagnosis given the potential for local outbreaks and costs to public health.

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0% found this document useful (0 votes)
84 views5 pages

Jurnal Resume 1

Hepatitis A is a common cause of acute hepatitis spread through the fecal-oral route. This case report describes a 30-year-old male who presented with jaundice and flu-like symptoms and was found to have hepatitis A infection based on laboratory testing showing significant liver inflammation. While hepatitis A generally causes a self-limited illness, this case illustrates the importance of considering the diagnosis given the potential for local outbreaks and costs to public health.

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Foster, DO A, Hernandez, DO S.

Hepatitis A: A Case Report Example of a Growing


Epidemiological Threat. SMRJ. 2019;3(3).

Case Report

Hepatitis A: A Case R
Report
eport Example of a Gro
Growing
wing Epidemiological Threat
* †
Adam Foster, DO , Stephanie Hernandez, DO
Keywords: public health, epidemiology, jaundice, hepatitis a

Spartan Medical R
Research
esearch Journal
Vol. 3, Issue 3, 2019

Hepatitis A is a common worldwide cause of acute hepatitis. It has been classically


associated with epidemics and is increasingly prevalent in the developing world.
Generally, the illness is self-limited and only requires supportive management,
reassurance, and proper hygiene instructions. This case involves a male in his early
30s who presented non-emergently with jaundice and a weeklong history of fatigue,
nausea, and flu-like symptoms. The patient underwent laboratory and radiological
evaluation. Test results revealed a significant transaminitis, hyperbilirubinemia, and
suggestion of cholecystitis. Further testing did reveal hepatitis A infection. This case
illustrates the importance of clinicians having a high clinical suspicion for the disease
based on individual risk factors as this disease can have a profound epidemiological
impact in terms of local outbreaks and public health expenses.

INTR
INTRODUC
ODUCTION
TION precautions and prevention of complications. Primary
and secondary prophylaxis is available, however
Hepatitis is a generic term that refers to some manner vaccination is not mandatory as the disease is rarely
of liver inflammation. The most common causes fatal, has no chronic carrier state, and has an overall
leading to such a diagnosis include viral infections low incidence in the United States.2
and chronic alcohol abuse.1 Other causes can include
bacterial, fungal, parasitic, immunologic, and toxic
METHODS
exposures. Hepatitis A Virus (HAV) is a virus that is
spread almost exclusively through the fecal-oral CASE REP
REPOR
ORT
T
route, although there does exist a very rare ability A Caucasian male in his early 30s presented to the ED
for blood transmission.1 HAV is an acute illness and with the chief complaint of yellowing of his skin and
there is no associated chronic carrier state (i.e., typically white sclera of his eyes. This was preceded by
asymptomatic person capable of transmitting) such five days of progressive fatigue and flu-like symptoms.
as seen with Hepatitis B Virus (HBV) or Hepatitis C He also admitted to having produced several tan-
Virus (HCV). Typically, cases occur in association with colored bowel movements, dark urine, subjective
epidemics, as opposed to sporadic cases, with the fevers, and nausea. He denied any abdominal pain,
most common risk factor for transmission being travel vomiting, diarrhea, hematuria, or rashes. He also
outside of the US.1 denied having completed any recent travel, insect or
chemical exposures, or any known sick contacts.
The incubation period for HAV ranges from 14 to 45
days, with a relatively short duration of viremia (i.e., He did not recall any peculiar food exposures during
detectable virus in the blood) and maximum the prior week. He denied ever having experienced
infectivity to others that is most prominent before symptoms like this in the past but did admit to current
symptom onset.1 Differentiation of the cause of HIV prophylaxis medication for the reason of "being
hepatitis generally requires a broad laboratory smart." He did admit to previous intravenous drug use
evaluation and thorough history and physical exam. with last administration three years prior. He had a
history of mild well-controlled asthma and denied any
Although HAV is rarely diagnosed initially in the previous surgeries.
Emergency Department (ED) due to serology testing
times,1 a high clinical suspicion for the disease can The patient's immediate vitals revealed hemodynamic
lead to timely intervention including contact stability with heart rate of 106, respiratory rate of 18,

* Institution: McLaren Macomb Department: Emergency Medicine


† Institution: McLaren Macomb Department: Emergency Medicine
Hepatitis A: A Case Report Example of a Growing Epidemiological Threat

Table 1 Emergency Department Laborator


Laboratoryy Evaluation
White Blood Cell 4.09 x103 per µL (normal range 4.0-10) Sodium 132 mEq/L
(135-145)
Hemoglobin 16.3 g/dL Potassium 3.8 mEq/L
(13-17) (3.5-5)
Platelets 88 x103 per µL (150-400) Chloride 95 mEq/L
(95-105)
Carbon Dio
Dioxide
xide 25 mEq/L
(20-29)
HIV
HIV,, Rapid Non-reactive Blood Urea Nitrogen 15 mg/dL
(8-21)
Influenza A/B Negative Glucose 451 mg/dL
(65-110)
Creatinine 0.990 mg/dL
(0.8-1.3)
Alkaline Phosphatase 484 U/L Prothrombin/INR 15.9 sec/1.54
(50-100) (11-14)/(0.9-1.2)
Bilirubin, total 9.20 mg/dL Calcium 8.00 mg/dL
(0.1-1.2) (8.5-10.2)
Bilirubin, direct 7.78 mg/dL Lactic Acid 1.4 mmol/L
(<0.3) (0.5-2.0)
Bilirubin, indirect 1.42 mg/dL
(<0.7)
Aspartate T
Trransaminase 2238 U/L
(5-30)
Alanine T
Trransaminase 3806 U/L
(5-30)
Lipase 193 U/L
(10-150)

temperature of 97.6 degrees axillary, blood pressure of evaluation was obtained to evaluate for the degree
140/86, and oxygen saturation of 100% on room air. of liver impairment and was pertinent for
His physical exam revealed a well-nourished, diffusely thrombocytopenia (88,000), hyperglycemia (451 mg/
jaundiced male in no acute distress. The patient was dL), hyperbilirubinemia (9.2 mg/dL), transaminitis
alert and oriented and answering all questions (2238 U/L and 3806 U/L), and elevated PT-INR (i.e.,
appropriately, albeit with short answers. prothrombin time-international normalized ratio) of
15.9 sec/1.54. (Table 1). These laboratory
Further examination revealed prominent bilateral abnormalities suggested possible new-onset Diabetes
yellow discoloration of the eyes (i.e., scleral icterus) Mellitus as well as significant liver dysfunction.
and abdominal examination demonstrated a mildly
distended abdomen with mild tenderness in the right Given the radiological findings and suspicion for
upper quadrant. There were no other indications of obstructive jaundice with possible gall bladder
peritonitis and the remainder of the physical infection (i.e., cholecystitis), the authors discussed
examination was within normal limits. The patient the case with general surgery. Orders for a magnetic
was provided with intravenous (IV) fluids and a broad resonance cholangiopancreatography (MRCP) and a
laboratory evaluation and computerized axial viral hepatitis panel were placed for suspected
tomography (CT) of the abdomen and pelvis with IV concomitant acute hepatitis. The patient was initiated
contrast was obtained. on IV antibiotics for suspected cholecystitis.

CT of the abdomen and pelvis was interpreted as gall The case was then discussed with the
bladder contraction with wall edema and mucosal Gastroenterology (GI) service who had also
hyper-enhancement. (Figure 1) No gallstones were recommended a MRCP, avoidance of hepatotoxic
identified and the liver, common bile duct and medications (e.g., acetaminophen and ciprofloxacin)
pancreas were all within normal limits. Laboratory and hepatitis panel. The patient was subsequently

Spartan Medical Research Journal 2


Hepatitis A: A Case Report Example of a Growing Epidemiological Threat

admitted to the hospital in hemodynamically stable


status with MRCP and hepatitis panel pending.
Gastrointestinal (GI), general surgery and
endocrinology for suspected new-onset Diabetes
Mellitus were consulted on the case.

During the patient's two-day hospital course, he


underwent a MRCP which showed no gallstones (i.e.,
cholelithiasis), intra or extra-hepatic biliary
dilatation, choledocholithiasis, or pancreatic ductal
dilatation. The patient's newly diagnosed Diabetes
Mellitus (Hemoglobin A1c of 9.2) was managed by
Endocrinology. A hepatitis panel indicated no
evidence of HBV or HCV reactivity but was reactive
for anti-HAV immunoglobulin (IgM), suggesting acute
HAV.

The patient was again evaluated by the same Figure 1 C


CT
T Abdomen/P
Abdomen/Pelvis
elvis Axial Slic
Slicee
consulting services with further recommendations of Demonstrating Gall Bladder C
Contrac
ontraction
tion with W
Wall
all
no surgical intervention being required and trending Thick
Thickening
ening
of the hepatic function panel. On the patient's
hospital Day 2, his repeat hepatic function lab panel
revealed improvement in the patient's liver enzymes abnormalities may be present, especially with
and function as well as his PT-INR. The patient was concomitant vomiting, such as orthostatic
subsequently discharged after receiving medical hypotension and tachycardia.
clearance from the consultants with strict clinic-based
follow-up. This entailed appropriate counseling with When managing a patient presenting with jaundice
regards to risk factor modification as well as ensuring and suspicion for hepatitis, it is especially important
resolution of jaundice and viral shedding. to gather a thorough history from the patient and
their recent contacts if possible. This history should
DISCUSSION include any known sick contacts, travel history, illicit
drug use, animal exposures, family history, or similar
Patients affected by HAV can have a highly variable occurrences in the past. Any of these risk categories
clinical presentation ranging from asymptomatic to should lead clinicians to suspect some form of
fulminant (i.e., a severe sudden onset) liver failure.1 hepatitis as a cause of the patients' presenting
A significant number of those patients affected are symptoms.
actually asymptomatic, but malaise, fever, and
anorexia are the most common presenting symptoms Clinicians being aware of current local
if they occur.1 These vague symptoms are generally epidemiological trends can also be of diagnostic
followed by nausea, vomiting, diarrhea, abdominal benefit. As of the time of this writing, there had been
discomfort, and the eventual development of a dramatic rise in the number of reported cases of
jaundice.3 Fulminant HAV, on the other hand, is acute HAV in Southeastern Michigan. The Michigan
exceedingly rare occurring in only 1-2% of cases.4 This Department of Health and Human Services had
is characterized by hepatic failure and progressive reported that as of 3/21/18 (beginning 8/1/16) there
encephalopathy (i.e., brain pathology) over a period of have been 789 reported cases of HAV related to the
days.4 outbreak.5 This condition contributed to 635
hospitalizations (80.5%) and 25 deaths (3.2%).
Patients may also present with rare and specific
symptoms as in this case including pale (i.e., acholic) Of note, Macomb County has the highest number of
stools and dark urine, both of which are indicative reported cases at 212 cases which is more than the city
of a conjugated hyperbilirubinemia. This suggests an of Detroit (i.e, 166 cases).5 The outbreak is believed
inability of the liver to expel bilirubin from the bile to be linked to county-wide opioid and heroin use
ducts, either from intrinsic hepatocyte dysfunction or patterns as over half of the reported cases has some
an external obstruction or both. This is compared to connection with this factor. As in this case, our patient
an unconjugated hyperbilirubinemia that would admitted to a history of IV drug use and as was later
typically suggest an abundance of bilirubin being determined during his hospitalization he also
produced for a myriad of reasons.3 Physical admitted to engaging in other high-risk behaviors
examination findings typically include scleral and/or including sex with other men.6
cutaneous icterus, abdominal tenderness and palpable
hepatomegaly.3 Aside from fever, other vital sign The economic impact of HAV outbreaks has been
reviewed both globally as well as on a national level.

Spartan Medical Research Journal 3


Hepatitis A: A Case Report Example of a Growing Epidemiological Threat

One 2003 study in particular looked at a Spokane, Control (CDC) guidelines, unvaccinated persons who
Washington outbreak and estimated each case of HAV have been exposed recently to HAV should be
cost $2,683.7 Most of the expenditures were associated administered one dose of the single-antigen HAV
with hospital admissions and lost productivity in the vaccine or immune globulin (IG) as soon as possible
community was also a major indirect factor. The and within two weeks after exposure.9 IG is preferred
expense of these endemics when compared to for those less than 12 months old and greater than 40
vaccination programs and other preventative public years old, immunocompromised persons with chronic
health initiatives continues to be an area of liver disease, and those who are allergic to the
epidemiological interest.8 vaccine.9

A HAV diagnosis is typically not made in the ED but As for primary prophylaxis, the CDC and the Advisory
suspected cases can be managed expectantly (i.e., Committee on Immunization Practices (ACIP)
monitored closely before treatment) while definitive recommends that all children at one year of age, those
studies are pending. The differential diagnosis at increased risk for infection or complications from
includes bacterial, viral, fungal, parasitic, and HAV, and any person wishing to obtain immunity
alcoholic hepatitis.1 Also included are causes of extra- should receive the vaccination.6 The HAV vaccine has
hepatic obstruction such as cholelithiasis, been available since 1995 and has resulted in a 95%
cholecystitis, choledocholithiasis, and malignancy of decline in the incidence of disease.6 Despite the
the biliary and pancreatic tissue.1 Diagnostic imaging apparent success of the vaccine, mandatory
is usually indicated in the form of a right upper administration is not the norm owing largely to the
quadrant ultrasound and possible CT of the abdomen fact that the disease is rarely fatal, has no chronic
and pelvis.3 carrier state, and has an overall low incidence in the
United States.2
More advanced imaging may be indicated in the form
of a MRCP to further distinguish biliary pathology and CONCLUSIONS
possibly intervene on a cause of obstruction. The most
critical laboratory studies to obtain include a hepatic In this paper, the authors reported on the presentation
function panel to assess degree of liver enzyme of a patient with an acute HAV infection. A
elevation (transaminitis), hyperbilirubinemia, and PT- presumptive diagnosis of hepatitis was made in the
INR which serves as the most accurate representation ED based on the patient's historical risk factors with
of hepatic impairment.4 Definitive studies for acute symptomatology, coupled with supporting laboratory
HAV (as well as HBV and HCV) can be obtained findings. The case was complicated by the findings on
through a viral hepatitis panel. Acute HAV is indicated imaging suggestive of acute cholecystitis. Appropriate
by positive Anti-HAV IgM whereas IgG indicates past lab value serologies were obtained and supportive care
exposure (when not co-existing with IgM).9 was provided which resulted in a short hospital
admission with gradual improvement in symptoms
Management of acute HAV includes IV fluids and and liver function. This case illustrates the importance
electrolyte correction, anti-emetics, and avoidance of of clinicians observing a broader differential diagnosis
hepatotoxic medications (e.g., acetaminophen and as well as having an understanding of the illness
ciprofloxacin) and alcohol intake.1 Antiviral and course and possible complications. This case report
antibiotic medications are not indicated in example further stresses the significance of clinicians
uncomplicated acute HAV.1 Hospitalization is considering local epidemiological trends and how this
generally reserved for those with intractable vomiting, may aid in diagnosis and appropriate management
severe electrolyte or fluid imbalance, altered mental thereafter.
status, a PT-INR greater than 1.5, or any other
evidence of fulminant disease.1 Otherwise stable The authors report no external funding source for this
individuals can be safely discharged with a study.
presumptive diagnosis and strict clinic-based
gastroenterology follow-up. Patients should be The authors declare no conflict of interest.
instructed on strict hand hygiene and those working
in the food industry should delay return to work until Submitted for publication September 2018.
their jaundice has resolved.6
Accepted for publication December 2018.
According to the latest federal Centers for Disease

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License
(CCBY-4.0). View this license’s legal deed at http://creativecommons.org/licenses/by/4.0 and legal code at
http://creativecommons.org/licenses/by/4.0/legalcode for more information.

Spartan Medical Research Journal 4


Hepatitis A: A Case Report Example of a Growing Epidemiological Threat

REFERENCES

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Elsevier; 2018. titis/hav/havfaq.htm#general.

2. Vaccines.gov. Hepatitis A. https://www.vaccines.go 7. Bownds L, Lindekugel R, Stepak P. Economic impact


v/diseases/hepatitis_a/index.html. Accessed of a hepatitis A epidemic in a mid-sized urban
November 10, 2018. community: the case of Spokane. Washington J
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Comprehensive Study Guide. 8th ed. New York: Hepatitis A: Epidemiology and prevention in
McGraw-Hill Education; 2016:525-531. developing countries. World J Hepatol.
2012;4(3):68-73.
4. Lee HW, Chang D-Y, Moon HJ, Chang HY, Shin E-C,
Lee JS, et al. Clinical Factors and Viral Load 9. Kingery JE, Matheny SC. Hepatitis A. Am Fam
Influencing Severity of Acute Hepatitis A. PLoS ONE. Physician. 2012;86(11):1027-1034.
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5. Michigan.gov. MDHHS Michigan Hepatitis A


Outbreak. https://www.michigan.gov/mdhhs/0,588
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0.html.

Spartan Medical Research Journal 5

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