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eMedicine Specialties > Emergency Medicine > Gastrointestinal

Viral Hepatitis

Adrienne M Buggs, MD, FACEP, FAAEM,, Medical Director, Drug Enforcement Administration Training Academy Health Unit; Consulting Staff, Department of Emergency Medicine, Dewitt Army Hospital
Joseph K Lim, MD, Assistant Professor of Medicine, Director, Yale Viral Hepatitis Program, Section of Digestive Diseases, Yale University School of Medicine

Updated: Jul 7, 2009

Introduction

Background

Hepatitis is a general term that refers to inflammation of the liver. This condition may result from various infectious and noninfectious etiologies.

Infectious etiologies include viral, bacterial, fungal, and parasitic organisms. In the United States, viral hepatitis is most commonly caused by hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These 3 viruses can all result in an acute disease process with symptoms of nausea, abdominal pain, fatigue, malaise, and jaundice.[1 ]Additionally, HBV and HCV can also lead to chronic infection. Patients who are chronically infected may go on to develop cirrhosis and hepatocellular carcinoma.[1 ]Furthermore, chronic hepatitis carriers remain infectious and may transmit the disease for many years.[2 ]

Noninfectious hepatitis may result from medications, toxins, and autoimmune disorders. This article focuses on viral hepatitis.

Frequency

United States

The Centers for Disease Control and Prevention (CDC) conducts national surveillance for acute hepatitis A, B, and C. The most recent statistics compiled are based upon data collected from 2006. In 2006, 3579 cases of acute, symptomatic hepatitis A virus were reported. This is the lowest incidence of hepatitis A virus ever recorded and represents a 90% decline from annual cases reported from 1995 through 2005. Because a good deal of hepatitis A virus infections may be asymptomatic or may go unreported, the CDC estimates the actual number of new hepatitis A virus infections in 2006 to be about 32,000.[1 ]

For hepatitis B virus, 4713 acute, symptomatic cases were reported for year 2006. This is the lowest rate ever recorded. With correction for asymptomatic cases and underreporting, the true number is estimated at 46,000 new infections in 2006.[1 ]

In contrast, the number of confirmed cases of acute hepatitis C increased in the year 2006. Approximately 802 cases were reported, with the actual numbers estimated at around 19,000 new hepatitis C virus infections in 2006.[1 ]

International

Annually, hepatitis A virus is responsible for an estimated 1.4 million infections worldwide.[3 ]Hepatitis B virus causes more than 4 million cases of acute hepatitis per year throughout the world, and it is estimated that approximately 350 million people are chronically infected with hepatitis B virus.[2 ]For hepatitis C virus, the worldwide annual incidence of acute infection is not easily estimated because patients are often asymptomatic. An estimated 170 million people are chronically infected with hepatitis C virus worldwide.[4 ]

Mortality/Morbidity

Chronic infection with hepatitis B virus is responsible for approximately 5000 deaths per year from chronic liver disease in the United States. An estimated 8,000-10,000 chronic liver disease deaths occur as a result of hepatitis C virus infection.[1 ]

Clinical

History

Clinical presentation of infectious hepatitis varies from person to person as well as with the etiology of infection. Some patients may present as entirely asymptomatic or only mildly symptomatic. Others may present with rapid onset of fulminant hepatic failure. The classic presentation of infectious hepatitis involves 4 phases.

  • Phase 1 - Viral replication
    • Patients are asymptomatic during this phase.
    • Laboratory studies demonstrate serologic and enzyme markers of hepatitis.
  • Phase 2 - Prodromal phase
    • Patients experience anorexia, nausea, vomiting, alterations in taste, arthralgias, malaise, fatigue, urticaria, and pruritus. Some develop an aversion to cigarette smoke.
    • When seen by a health care provider during this phase, patients are often diagnosed as having gastroenteritis or a viral syndrome.
  • Phase 3 - Icteric phase
    • Patients may note dark urine, followed by pale-colored stools.
    • In addition to the predominant gastrointestinal symptoms and malaise, patients become icteric and may develop right upper quadrant pain with hepatomegaly.
  • Phase 4 - Convalescent phase
    • Symptoms and icterus resolve.
    • Liver enzymes return to normal.

Physical

  • Physical findings in patients with hepatitis vary with the type of hepatitis and time of presentation.
  • Patients often present with low-grade fever.
  • Patients experiencing significant vomiting and anorexia may show signs of dehydration such as tachycardia, dry mucous membranes, loss of skin turgor, and delayed capillary refill.
  • Patients in the icteric phase may have icterus of the sclerae or mucous membranes or discoloration of the tympanic membranes.
  • The skin may be jaundiced and may reveal macular, papular, or urticarial rashes.
  • In viral hepatitis, the liver may be tender and diffusely enlarged with a firm, sharp, smooth edge.
  • If the patient has a nodular liver or a mass is palpated, clinicians should be suspicious for an abscess or tumor.

Causes

  • Infectious hepatitis, viral
    • Five major hepatotropic viruses cause the majority of clinical cases of viral hepatitis. These are hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV).
    • HAV, HBV, and HCV cause more than 90% of cases of acute viral hepatitis in the United States.
    • Hepatitis viruses A, B, C, and D are the only hepatitis viruses endemic to the United States.
  • Hepatitis A
    • Epidemiology: HAV is a picornavirus that is resistant to many environmental factors (eg, temperature, certain chemicals). Often, the predominant etiologic agent of viral hepatitis in the United States, HAV accounts for 25-50% of new cases per year. Based on 2006 CDC data, HAV was responsible for approximately 32% of new cases of viral hepatitis in the United States.[1 ]
    • Transmission
      • Hepatitis A virus exists in highest concentration in the feces of infected individuals; the greatest fecal viral load tends to occur near the end of the incubation period of hepatitis A virus.
      • Most commonly, the virus spreads from person to person via the fecal-oral route. Contaminated water and food, including shellfish collected from sewage-contaminated water, have also resulted in epidemics of hepatitis A virus.
      • The virus may also be spread through sexual (anal-oral) contact.[3 ] 
      • Transmission by blood transfusion is rare.[3 ]
      • Infection with hepatitis A virus occurs throughout the world. However, risk of infection is greatest in developing countries, areas of low socioeconomic status, and areas without sufficient sanitation. Higher infection rates also exist in settings where fecal-oral spread is likely, such as daycare centers.[1 ]
      • Other groups at high risk for hepatitis A virus infection include international travelers, users of injection and noninjection drugs, and men who have sex with men.[1,3 ]International travel was the most frequently identified risk factor reported by case patients in the United States in 2006.
      • Maternal-neonatal transmission has not been established.[3 ]
      • Close contacts of infected individuals are also at risk.[1 ]The secondary infection rate for hepatitis A virus in household contacts of patients with acute hepatitis A virus infection is around 20%. Thus, secondary infection plays a significant role in the maintenance of hepatitis A virus outbreaks.
    • Clinical course
      • The incubation period of hepatitis A virus is 2-7 weeks, with an average of 28 days. Clinical symptoms then develop, often with a presentation similar to that of gastroenteritis or a viral respiratory infection.
      • Most common signs and symptoms include fatigue, nausea, vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, and rash.
      • Hepatitis A virus infection usually occurs as a mild self-limited disease and confers lifelong immunity to hepatitis A virus. Chronic infection with hepatitis A virus does not occur.
    • Morbidity and death
      • Although hepatitis A virus usually causes mild disease, older patients are at greater risk for severe disease. While icteric disease occurs in fewer than 10% of children younger than 6 years, it occurs in 40-50% of older children and in 70-80% of adults with hepatitis A virus. Other complications can include acute liver failure, cholestatic hepatitis, and relapsing hepatitis.
      • The overall mortality rate for hepatitis A virus is approximately 0.01%. Children younger than 5 years and adults older than 50 years have the highest case-fatality rates.
  • Hepatitis B
    • Epidemiology
      • A major cause of infectious hepatitis worldwide, hepatitis B virus belongs to the class of hepadna viruses. Hepatitis B virus is responsible for almost half of the cases of acute viral hepatitis cases reported in the United States. In 2006, the highest rates of acute infection occurred in patients aged 25-44 years.[1 ] 
      • Estimates suggest that 350 million people worldwide are hepatitis B virus carriers.[2 ]The virus leads to 1 million deaths annually as a result of viral hepatitis – induced liver disease.[2 ]
      • The incidence of childhood hepatitis B virus infection is not well established because more than 90% of hepatitis B virus infections in this age group are asymptomatic.
    • Transmission
      • The major reservoir of hepatitis B virus in the United States consists of the 1.25 million people with chronic hepatitis B virus infection.[1 ]In this group, those with hepatitis B e antigen (HBeAg) in their serum tend to have higher viral titers and thus greater infectivity.
      • Hepatitis B virus is transmitted both parenterally and sexually, most often by mucous membrane exposure or percutaneous exposure to infectious body fluids. Saliva, serum, and semen all have been determined to be infectious.
      • Percutaneous exposures leading to the transmission of hepatitis B virus include transfusion of blood or blood products, injection drug use with shared needles, hemodialysis, and needlesticks (or other wounds caused by sharp implements) in health care workers.
      • Globally and in the United States, perinatal transmission is one of the major modes of transmission. The greatest risk of perinatal transmission occurs in infants of HBeAg-positive women. By age 6 months, these children have a 70-90% risk of infection and, of those, about 90% will go on to develop chronic infection with hepatitis B virus.
      • For infants born to HBeAg-negative women, risk of infection approximates 10-40%, with a chronic infection rate of 40-70%. Even if transmission does not occur in the perinatal period, these children still have a significant risk of developing infection during early childhood.
      • High-risk groups for infection with hepatitis B virus include intravenous drug users, persons born in endemic areas, and men who have sex with men.[2 ]
      • Other groups at risk include health care workers with exposure to infected blood or bodily fluids, recipients of multiple blood transfusions, patients undergoing hemodialysis, heterosexual persons with multiple partners or a history of sexually transmitted disease, institutionalized persons including prisoners, people who are developmentally disabled, and household contacts or sexual partners of HBV carriers.[2 ]
    • Clinical course
      • The incubation period for hepatitis B virus varies from 30-180 days, with the average approximately 75 days. Patients then enter the prodromal or preicteric phase, developing gradual onset of anorexia, malaise, and fatigue. During this phase, as the liver becomes inflamed, liver enzymes start to elevate, and the patient may experience right upper quadrant pain. Fifteen percent of patients develop an illness resembling serum sickness. These patients may experience fever, arthritis, arthralgias, or an urticarial rash.
      • As the disease progresses to the icteric phase, the liver becomes tender, and jaundice develops. Patients may note that their urine darkens and that their stools lighten in color. Other symptoms in this stage include nausea, vomiting, and pruritus.
      • From this point on, patients may have quite a variable course. Some experience fairly rapid improvements in their symptoms, while others go on to a prolonged disease course with slow resolution. Still others may have symptoms that periodically improve, only to worsen later (relapsing hepatitis).
      • Finally, an unfortunate subset of patients suffers rapid progression of their disease to the point of fulminant hepatic failure. This may occur over days to weeks.
    • Complication
      • One of the major complications of hepatitis B virus infection is the development of chronic infection. An estimated 350 million people worldwide are chronically infected with hepatitis B virus.[2 ] In the United States, 1.25 million people are estimated to have chronic hepatitis B virus infection.[1 ]Patients with chronic HBV infection are at risk of later developing chronic active hepatitis, cirrhosis of the liver, and eventual hepatocellular cancer. Each year, approximately 1 million deaths occur worldwide as a result of chronic hepatitis B virus infection.[2 ]
      • Patients infected at an early age have the greatest risk of developing chronic hepatitis B virus infection. While 90% of those infected at birth develop chronic hepatitis B virus, only 5-10% of older children or adults go on to develop chronic infection.[2 ]The risk of chronic infection is also higher in patients who are immunocompromised.
      • Patients with chronic hepatitis B virus infection have a significantly increased risk of developing hepatocellular cancer. In fact, hepatocellular cancer is the leading cause of cancer-related deaths in areas where hepatitis B virus is endemic. Globally, hepatitis B virus is responsible for 60-80% of the world’s primary liver cancers.[2 ] Cancer in this setting is postulated to result from repeated bouts of chronic inflammation and cellular regeneration. Hepatocellular cancer develops an average of 25-30 years after initial infection.
      • Another major complication of hepatitis B virus infection is development of fulminant hepatic failure. In approximately 0.5-1% of HBV-infected patients, the disease progresses to fulminant hepatic failure, with coagulopathy, encephalopathy, and cerebral edema. The case-fatality rate for these patients approaches 80%.[2 ]
  • Hepatitis C
    • Epidemiology
      • Hepatitis C is a single-stranded ribonucleic acid (RNA) virus that is the most frequent cause of parenteral non-A, non-B hepatitis worldwide. Estimates suggest that, worldwide, 170 million people are chronically infected with hepatitis C virus.[1 ]In the United States, approximately 3.2 million people have chronic hepatitis C virus infection.
      • Hepatitis C virus causes approximately 20% of acute viral hepatitis cases in the United States per year, and the CDC estimates that 150,000 new cases of HCV occur annually.[1 ]
      • Highest rates of disease prevalence are found in patients with hemophilia and in injection drug users. Before the newer universal plasma and donor screening measures, hepatitis C virus accounted for 90% of post-transfusion hepatitis cases.[5,4 ]
      • Hepatitis C virus is the most common cause of chronic viral hepatitis in the United States. About 70-90% of people infected progress to chronic hepatitis C virus infection.[4 ]
    • Transmission
      • Hepatitis C virus can be transmitted parenterally, perinatally, and sexually. Transmission occurs by percutaneous exposure to infected blood and plasma.[4 ]
      • Hepatitis C virus is transmitted most reliably through transfusion of infected blood or blood products, transplantation of organs from infected donors, and sharing contaminated needles among intravenous drug users.[4 ]
      • Transmission by sexual activity and household contact occurs less frequently.[4 ]
      • Perinatal transmission occurs but is uncommon.[4 ]
    • Clinical course
      • Incubation period for hepatitis C virus runs 15-150 days, with symptoms developing anywhere from 5-12 weeks after exposure.
      • During acute infection with hepatitis C virus, symptoms may appear similar to those of hepatitis B virus infection.
      • In up to 80% of cases, however, patients are asymptomatic and do not develop icterus.[1,4 ]
    • Complications
      • Acute infection with hepatitis C virus may rarely cause fulminant hepatic failure.[4 ]
      • Approximately 70-90% of patients with hepatitis C virus become chronically infected. More than 60% of patients will have ongoing chronic liver disease with laboratory evidence of fluctuating or persistently elevated liver enzymes.
      • Of those with chronic infection, 5-20% may go on to develop cirrhosis. The progression from initial infection to the development of cirrhosis may take more than 20 years.[4 ]
      • Cirrhosis related to chronic hepatitis C virus infection is also strongly linked to the development of hepatocellular cancer, which usually develops after 30 years in patients who are chronically infected. Of patients with HCV-associated cirrhosis, 20-25% may progress to liver failure and death.[4 ] 
      • In the United States, cirrhosis associated with chronic hepatitis C virus infection is a leading indication for liver transplant.[4 ]
  • Hepatitis D
    • Epidemiology
      • Hepatitis D virus is a defective, single-stranded RNA virus that requires the presence of hepatitis B virus to replicate. Hepatitis D virus infection develops only in patients who are positive for the hepatitis B surface antigen (HBsAg).[6 ]
      • Patients may acquire hepatitis D virus as a co-infection (at the same time that they contract hepatitis B virus), or the hepatitis D virus may super-infect patients who are chronic hepatitis B virus carriers.
      • Although hepatitis D virus is not a reportable disease, the CDC estimates that it results in 7500 infections each year. Approximately 4% of cases of acute hepatitis B virus are thought to involve co-infection with hepatitis D virus.
    • Transmission: Modes of transmission for hepatitis D virus are similar to those for hepatitis B virus.
      • Hepatitis D virus is transmitted by exposure to infected blood and blood products. It can be transmitted percutaneously and sexually.[7 ]
      • Perinatal transmission is rare.[7 ]
    • Clinical course
      • The incubation period of hepatitis D virus is approximately 35 days.
      • Patients co-infected (simultaneously infected) with hepatitis B virus and hepatitis D virus often have an acute, self-limited infection.[7,6 ] Less than 5% of these patients develop chronic hepatitis D virus infection.
      • Chronic hepatitis B virus carriers who become super-infected with hepatitis D virus tend to have a more severe acute hepatitis; 80% of these patients go on to develop chronic HDV infection. Chronic infection with hepatitis B virus and hepatitis D virus may lead to fulminant acute hepatitis and severe chronic, active hepatitis with progression to cirrhosis.[7,6 ]
      • Over the long term, as many as 70-80% of these patients have evidence of chronic liver disease with cirrhosis, compared to only 15-30% of patients with chronic hepatitis B virus alone.
  • Hepatitis E
    • Epidemiology
      • Hepatitis E virus is the primary cause of enterically transmitted non-A, non-B hepatitis; most outbreaks occur in developing countries.
    • Transmission
      • Hepatitis E virus is transmitted primarily by the fecal-oral route, with fecally contaminated water providing the most common means of transmission.[8,9 ]
      • Person-to-person transmission is rare.[9 ]
      • Maternal-neonatal transmission does occur.[9 ]
      • Zoonotic spread is possible as some nonhuman primates (cows, pigs, sheep, goats, and rodents) are susceptible to the disease.[8 ]
    • Clinical course
      • The incubation period of hepatitis E virus is 2-9 weeks, with an average of 45 days.
      • Hepatitis E virus usually causes an acute self-limited disease similar to hepatitis A virus. Fulminant disease does occur in about 10% of cases. In women who are pregnant, hepatitis E virus infection has a case-fatality rate of 15-20%.[9 ]
      • No reports exist of chronic infection with hepatitis E virus.[9 ]
  • Other types of viral hepatitis
    • Hepatitis G virus, characterized in 1996, is associated with acute and chronic liver disease, but studies have not clearly implicated hepatitis G virus as an etiologic agent of hepatitis. It is transmitted through blood and blood products.[9 ]
    • Other known viruses (eg, cytomegalovirus, Epstein-Barr virus, herpes simplex, varicella-zoster) may also cause inflammation of the liver, but they do not primarily target the liver.
  • Infectious hepatitis, nonviral
    • Hepatic abscesses may cause infectious hepatitis. These occur more often in patients with chronic illness. The two general categories of abscess are amebic (most commonly caused by Entamoeba histolytica in developing countries) and pyogenic (tending to affect those at the extremes of age).
    • In neonates, sepsis and catheterization of the umbilical vein may result in abscesses caused by gram-positive aerobic cocci.
    • In adults, biliary disease can result in pyogenic abscess formation with the mortality rate of pyogenic abscesses at almost 40%. Gram-negative rods are the typical causative organisms in adults.
    • In elderly persons, malignancy is the most common underlying disease.

Differential Diagnoses

Abdominal Trauma, Blunt
Obstruction, Small Bowel
Aneurysm, Abdominal
Pancreatitis
Cholangitis
Pediatrics, Gastroenteritis
Cholecystitis and Biliary Colic
Pediatrics, Intussusception
Cholelithiasis
Gastritis and Peptic Ulcer Disease
Gastroenteritis

Other Problems to Be Considered

Liver abscess
Drug-induced hepatitis
Autoimmune hepatitis
Hepatocellular cancer
Pancreatic cancer

Workup

Laboratory Studies

  • A simple screening test for the nonicteric patient with suspected viral hepatitis involves checking the urine for presence of bilirubin. As an alternative, a liver enzyme panel (generally a costly test) could be obtained.
  • Bedside fingerstick glucose testing is important in evaluating for hypoglycemia in patients with an altered or questionable mental status.
  • Serum bilirubin (total and fractionated): Total bilirubin may be elevated in infectious hepatitis. Bilirubin levels higher than 30 mg/dL indicate more severe disease.
  • Alkaline phosphatase usually is in the reference range but may elevate to no higher than twice the normal level. If alkaline phosphatase is elevated significantly, consider abscess or biliary obstruction.
  • Prothrombin time (PT), if prolonged, is a grave finding indicating impaired synthetic function of the liver.
  • Draw BUN and serum creatinine to look for evidence of renal impairment. Decreased renal function suggests fulminant hepatic disease.
  • Measure serum ammonia in patients with altered mental status or other evidence of hepatic encephalopathy.
  • Hepatitis A antibody (immunoglobulin M [IgM] anti-HAV): Detecting the presence of IgM anti-HAV in serum is the standard for diagnosing acute infection with HAV.
  • Hepatitis B core antibody (IgM anti-HBc): Determining the presence of IgM anti-HBc in serum is required to make the diagnosis of acute HBV infection.
  • Hepatitis B surface antigen may be present in acute infection or in patients who are chronic carriers. Its presence in patients with symptoms of acute hepatitis strongly suggests acute HBV infection but does not rule out chronic HBV with acute superinfection by another hepatitis virus. The presence of HBsAg in the serum for 6 months or longer is indicative of chronic infection.
  • Hepatitis C infection can be confirmed with serologic assays to detect antibodies to HCV (anti-HCV) or by molecular tests for the presence of viral particles. The third-generation assays for anti-HCV are sensitive and specific and can detect such antibodies within 4-10 weeks of infection. The qualitative PCR assay for presence of viral particles is the most specific test of HCV infection and may be helpful in diagnosing acute HCV infection before antibodies have developed.
  • Assays to detect IgM antibody to HDV do not need to be routinely performed in all patients with suspected hepatitis.

Imaging Studies

  • No specific imaging studies are required to make the diagnosis of hepatitis.
  • Obtain the appropriate diagnostic imaging studies (eg, ultrasound, computed tomography) if the differential diagnosis favors gallbladder disease, biliary obstruction, or liver abscess.

Other Tests

  • Liver biopsy may be recommended for the initial assessment of disease severity in patients with chronic hepatitis B or chronic hepatitis C.

Treatment

Emergency Department Care

  • Viral hepatitis: No specific emergency department treatment is indicated other than supportive care including intravenous rehydration.
  • A liver abscess requires intravenous antibiotic therapy directed toward the most likely pathogens and consultation for possible surgical or percutaneous drainage.

Consultations

  • Gastroenterologist or hepatologist
  • General surgeon

Medication

Certain patients may benefit from pharmacologic therapy. For chronic hepatitis B virus (HBV) and chronic hepatitis C virus (HCV) infections in particular, the goals of therapy are to reduce liver inflammation and fibrosis and to prevent progression to cirrhosis and its complications.

Because the treatment regimens for hepatitis are being actively researched, medication recommendations, indications, and dosages are all subject to change. Make any decision to administer medications in consultation with a gastroenterologist or a hepatologist.

In addition to the medications listed below, the nucleoside analogues lamivudine and adefovir have shown promising results in the treatment of patients with chronic HBV. Other antiviral agents that are being studied for treatment of chronic HBV include entecavir and tenofovir. In addition to being active against HBV, lamivudine, adefovir and tenofovir are also active against human immunodeficiency virus (HIV), making them useful in the treatment of patients who are co-infected with HBV and HIV.

For patients with chronic HCV infection, one current treatment option is combination therapy with pegylated interferon (PEG-IFN) and the antiviral ribavirin. This regimen may be recommended for a certain subset of patients with moderate or severe inflammation and/or fibrosis. The combination of the 2 drugs provides a more sustained clearance of HCV RNA from the serum of infected individuals when compared to monotherapy. Other therapeutic options are being explored for treatment of chronic HCV with the goals of increasing efficacy and decreasing toxicity. These include protease inhibitors, ribozymes, and viral vaccines.

Interferons

These are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alpha, beta, and gamma interferons may be given topically, systemically, and intralesionally.


Interferon alpha-2b (Intron A)

Protein product manufactured by recombinant DNA technology that uses genetically engineered Escherichia coli bacterium.
Mechanisms by which it exerts antiviral activity are not clearly understood; however, modulation of host-immune response may play an important role.
Induces remission in 25-50% of patients with chronic HBV and 40% of patients with chronic HCV and decreases abnormal aminotransferase concentrations in chronic HBV/HCV. Also may play a role in delaying or preventing development of hepatocellular cancer, independent of its antiviral effect, in patients with cirrhosis.

Dosing

Adult

5 million IU/d or 10 million IU 3 times/wk IM/SC for 16 wk; reduce dose by 50% if severe adverse reactions occur

Pediatric

Not established

Interactions

Interleukin-2 increases potential risk of renal failure; theophylline may increase toxicity by reducing clearance; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity

Contraindications

Documented hypersensitivity; anaphylactic sensitivity to mouse IgG, egg protein, or neomycin

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Depression and suicidal ideation may be adverse effects; infrequently, severe or fatal GI hemorrhage reported in association with therapy; prior to initiation of therapy, perform tests to quantitate peripheral blood hemoglobin, platelets, granulocytes, hairy cells, and bone marrow hairy cells; monitor periodically (eg, monthly) during treatment to determine response to treatment; if patient does not respond within 6 mo, discontinue treatment

Antivirals

These agents inhibit viral replication.


Amantadine (Symmetrel)

Antiviral agent that prevents penetration of virus into host by inhibiting uncoating of virus; may be useful in patients with HCV who do not respond to interferon.

Dosing

Adult

100 mg PO bid for 6 mo

Pediatric

Not established

Interactions

Drugs with anticholinergic or CNS stimulant activity increase toxicity; hydrochlorothiazide plus triamterene may increase plasma concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and those receiving CNS stimulant drugs; reduce dose in renal disease when treating Parkinson disease; do not discontinue this medication abruptly


Famciclovir (Famvir)

Prodrug that, when biotransformed into active metabolite penciclovir, may inhibit viral DNA synthesis/replication.

Dosing

Adult

500 mg PO tid

Pediatric

Not established

Interactions

Probenecid or cimetidine may increase toxicity; increases bioavailability of digoxin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or coadministration of nephrotoxic drugs


Entecavir (Baraclude)

Guanosine nucleoside analogue with activity against HBV polymerase. Competes with natural substrate deoxyguanosine triphosphate to inhibit HBV polymerase activity (ie, reverse transcriptase). Less effective for lamivudine-refractory HBV infection. Indicated for treatment of chronic hepatitis B infection. Available as tab and oral solution (0.05 mg/mL; 0.5 mg = 10 mL).

Dosing

Adult

Treatment for nucleoside naive: 0.5 mg PO qd 2 h ac or 2 h pc
CrCl 30-49 mL/min: 0.25 mg PO qd
CrCl 10-29 mL/min: 0.15 mg PO qd
CrCl <10 mL/min: 0.05 mg PO qd
Receiving lamivudine or lamivudine resistance: 1 mg PO qd 2 h ac or 2 h pc
CrCl 30-49 mL/min: 0.5 mg PO qd
CrCl 10-29 mL/min: 0.3 mg PO qd
CrCl <10 mL/min: 0.1 mg PO qd

Pediatric

<16 years: Not established
>16 years: Administer as in adults

Interactions

Not a substrate, inhibitor, or inducer of cytochrome P450; coadministration with drugs that reduce renal function (eg, aminoglycosides, cidofovir, cyclosporine) or that compete for active tubular secretion (eg, probenecid, salicylates) may increase serum concentration of either entecavir or coadministered drug

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Reduce dose with renal impairment; if on hemodialysis, administer afterwards; common adverse effects include headache, tiredness, dizziness, and nausea; may elevate liver enzyme levels; may cause lactic acidosis; severe acute exacerbations of hepatitis B may occur in patients who discontinue antihepatitis B therapy

Corticosteroids

These agents may be used in cholestatic HAV. A brief course may shorten the illness; however, it may be most effective in a milder disease.


Prednisone (Deltasone, Sterapred, Orasone)

Inactive and must be metabolized to active metabolite prednisolone; conversion may be impaired in patients with liver disease.

Dosing

Adult

5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve

Pediatric

4-5 mg/m2/d PO; alternatively, administer 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve

Interactions

Estrogens may decrease clearance; concurrent digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur

Follow-up

Further Inpatient Care

  • Admit patients with hepatitis if they are showing any signs or symptoms suggestive of severe complications.
  • Admit and evaluate for hepatic encephalopathy any patients with altered mental status, agitation, behavior or personality changes, or changes in sleep-wake cycle.
  • Other admission criteria that are suggestive of severe disease include a PT prolonged greater than 3 seconds, bilirubin greater than 30 mg/dL, and hypoglycemia.
  • Admit any patients with intractable vomiting, significant electrolyte or fluid disturbances, or significant comorbid illness; those who are immunocompromised; and those who are older than 50 years.

Further Outpatient Care

  • Most patients with viral hepatitis can be monitored on an outpatient basis.
  • Ensure that patients are able to maintain adequate hydration, and arrange close follow-up care with their primary care physicians.
  • Instruct patients to refrain from using any potential hepatotoxins, such as ethanol or acetaminophen.
  • Advise patients to avoid prolonged or vigorous physical exertion until their symptoms improve.
  • Patients who are found subsequently to have hepatitis B virus or hepatitis C virus should be referred to a gastroenterologist or a hepatologist for further evaluation and treatment.

Deterrence/Prevention

  • Hepatitis A
    • Improved sanitation, strict personal hygiene, and hand washing all may help to prevent transmission of HAV. The virus is inactivated by household bleach or by heating to 85°C for 1 minute.
    • Travelers to endemic areas should not drink untreated water or ingest raw seafood or shellfish. Fruits and vegetables should not be eaten unless they are cooked or can be peeled.
    • Certain inactivated viral vaccines have proven highly effective in preventing infection with HAV when given before exposure. These vaccines are not recommended for children younger than 2 years. In this age group, passively acquired maternal anti-HAV antibodies may decrease the immunogenicity of the vaccine.
    • Active immunization is recommended for health care workers, daycare personnel, and travelers to endemic areas. HAV vaccine also is recommended for sewage and wastewater workers and veterinarians working with imported nonhuman primates.
    • Passive postexposure immunization with immune globulin (dose 0.02 mL/kg) can protect persons exposed to HAV against clinical illness.[10 ]Effectiveness is highest if given within 48 hours of exposure, but it may be helpful when given as far as 2 weeks into the incubation period. These patients also should receive active immunization with the HAV vaccine.
    • Immune globulin also is recommended before exposure for children younger than 2 years who are at risk of exposure to HAV.
  • Hepatitis B
    • Active immunization with the 3-dose recombinant DNA HBV vaccine may prevent infection. Recommendations from the Centers for Disease Control and Prevention are available on hepatitis B vaccination.[11 ]
    • Use of this vaccine has proven very successful in preventing infection among those at risk for HBV infection because of occupational exposure. Unfortunately, approximately 5-32% of those vaccinated do not develop an adequate antibody response to the HBV vaccine. Because of the nonresponse rate, many recommend that health care workers undergo postvaccination testing to confirm response within 1-2 months of receiving the vaccine. The duration of immunity conferred by the vaccine is not clearly known. Some authors recommend that a booster be given at 5-10 years.
    • This vaccine is recommended for all children as part of the usual immunization schedule as well as to infants born to mothers who are potentially infectious.
    • Nonimmunized persons who are close contacts of patients with acute HBV infection or who suffer percutaneous exposure to HBV, and infants born to potentially infectious mothers, should receive passive immunization with the HBV immune globulin in addition to active immunization.
    • Combined active and passive immunization in these settings is 80-95% effective in preventing transmission of HBV.
  • Hepatitis C
    • No vaccine against HCV is available, and immune globulin is not proven to prevent transmission. In fact, immune globulin administration has been associated with HCV.
    • At the present time, the major means of preventing transmission is to prevent infected blood, organs, and semen from entering the donor pools.
  • Hepatitis D
    • Since HDV can infect patients only when HBV is present, transmission of this disease can be decreased by effectively immunizing patients against HBV.
    • Unfortunately, at this time, no means is known of preventing HDV superinfection in patients with chronic HBV.
  • Hepatitis E
    • No vaccine exists for prevention of HEV.
    • Administration of immune globulin does not prevent development of clinical disease.

Complications

  • Acute/subacute hepatic necrosis
  • Chronic active hepatitis
  • Chronic hepatitis
  • Cirrhosis
  • Hepatic failure
  • Hepatocellular carcinoma (HBV, HCV)

Prognosis

The prognosis varies with causative virus.

  • Hepatitis A virus
    • Hepatitis A virus infection usually is mild and self-limited.
    • Infection confers lifelong immunity against hepatitis A virus.
    • Three rare complications include relapsing hepatitis, cholestatic hepatitis, and fulminant hepatic failure.
    • Mortality rate for hepatitis A virus hepatitis is 0.01%.
  • Hepatitis B virus
    • Risk of chronic infection in infected older children and adults approaches 5-10%.
    • Patients with chronic hepatitis B virus infection are at risk for cirrhosis and hepatocellular cancer.
    • Fulminant hepatic failure develops in 0.5-1% of patients infected with hepatitis B virus; their case-fatality rate is 80%.
  • Hepatitis C virus
    • Chronic infection develops in 50-60% of patients with hepatitis C virus.
    • Chronically infected patients are at risk for chronic active hepatitis, cirrhosis, and hepatocellular cancer.
    • Chronic hepatitis C virus infection is the leading indication for liver transplant in the United States.
    • Chronic hepatitis C virus infection is responsible for 10,000 deaths each year in the United States.
  • Hepatitis D virus
    • Patients with chronic hepatitis B virus who are co-infected with hepatitis D virus also tend to develop chronic hepatitis D virus infection.
    • Chronic co-infection with hepatitis B virus and hepatitis D virus often leads to rapidly progressive subacute or chronic hepatitis with as many as 70-80% of these patients eventually developing cirrhosis.
  • Hepatitis E virus
    • Hepatitis E virus infection usually is mild and self-limited.
    • Case-fatality rate reaches 15-20% in pregnant women.
    • Hepatitis E virus infection does not result in chronic disease.

Patient Education

  • Refer patients with infectious hepatitis to their primary care providers for further counseling specific to their disease, as the specific etiologic virus is unlikely to be known at time of discharge from the ED.
  • Counsel patients regarding the importance of follow-up care to monitor for evidence of disease progression or development of complications.
  • Advise patients in general to exercise meticulous personal hygiene including strict hand washing.
  • Instruct patients not to share any articles with potential for contamination with blood, semen, or saliva, including needles, toothbrushes, or razors.
  • Inform food handlers suspected of having HAV not to return to work until their primary care physician can confirm that they are no longer shedding virus.
  • Instruct patients to refrain from using any hepatotoxins, including ethanol and acetaminophen.
  • For excellent patient education resources, visit eMedicine's Hepatitis Center; Liver, Gallbladder, and Pancreas Center; and Public Health Center. Also, see eMedicine's patient education articles Hepatitis A; Hepatitis B; Hepatitis C; Cirrhosis; Immunization Schedule, Children; and Immunization Schedule, Adults.

Miscellaneous

Special Concerns

  • Pregnancy
    • In general, none of the hepatitis viruses are known to be teratogenic.
    • Except in the case of HEV, the disease courses of the various hepatitis viruses are no different in pregnancy.
    • Treatment usually consists of supportive care. Patients with significant vomiting or dehydration may require admission for hydration as well as monitoring for fetal well-being and preterm uterine irritability.
    • Nonimmunized patients who are pregnant and exposed to HAV or HBV should receive active and passive immunization with the appropriate immune globulin and viral vaccine. Immune globulin, HBV immune globulin, HAV vaccine, and HBV vaccine all currently are approved for use during pregnancy.
    • Hepatitis A: HAV has an incidence of less than 1 per 1000 in pregnancy. HAV is not transmitted to the fetus in utero but may be transmitted to the neonate during delivery or during the postpartum period (fecal-oral route). Infants born to women infected with HAV during the third trimester should receive postexposure prophylaxis with immunoglobulin.
    • Hepatitis B: Acute infection with HBV occurs at a rate of 1-2 per 1000 pregnancies. In addition, 0.5-1.5% of pregnant women are chronic carriers of HBV. No evidence exists of transplacental infection; perinatal infection of the neonate usually occurs during delivery. Infants born to mothers who are chronic carriers of HBV or who acquire acute HBV infection during the third trimester should receive active and passive immunization. When these neonates receive HBV vaccine and immune globulin within 12 hours of delivery, the rate of vertical transmission decreases so that fewer than 5% of exposed neonates become chronic carriers.
    • Hepatitis C: The most common risk factor for HCV infection in pregnancy is history of substance abuse. Vertical transmission does occur, but the exact frequency of this occurrence is unknown.
    • Hepatitis D: Perinatal transmission rarely occurs.
    • Hepatitis E: The disease course of HEV may be more severe during pregnancy, with a high case-fatality rate, especially when the disease is contracted during the second or third trimester. Perinatal transmission occurs but with undetermined frequency. When vertical transmission of HEV does occur, it is associated with significant perinatal morbidity and death.
    • Alternatively, acute hepatitis occurring during pregnancy may also be caused by certain disease states of pregnancy. These conditions include HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), acute fatty liver of pregnancy, ruptured liver hematoma, and intrahepatic cholestasis of pregnancy.
  • Drug-induced hepatitis
    • A large number of prescription medicines, drugs, and chemical agents are known to cause hepatotoxicity. Some agents cause hepatic damage directly, while others induce an autoimmune response against the liver. Damage can occur acutely or from chronic exposure. Moreover, drug-induced hepatitis follows viral hepatitis as a leading cause of fulminant hepatic failure in the United States.
    • Prescription medications that have been associated with drug-induced hepatitis include acetaminophen, amiodarone, amoxicillin-clavulanate, minocycline, nitrofurantoin, telithromycin, trimethoprim-sulfa, and trovafloxacin. Hepatitis induced by medications accounts for up to 5% of hospitalizations for hepatitis in the United States.
    • Various herbal preparations and toxic plants have been implicated in causing hepatitis. Some products that have been associated with significant hepatotoxicity include Comfrey, Germander, Jin Bu Huan, Kava, Ma Huang, Pennyroyal, Senna, and Valerian.
    • Several drugs of abuse are known to cause hepatic injury, including cocaine, methylenedioxymethamphetamine (ecstasy), toluene, trichloroethylene, phencyclidine, and ethanol. Patients hospitalized with hepatitis induced by ethanol have a reported mortality rate of 20-65%.
    • Occupational exposure to a variety of industrial agents may produce liver injury.
    • Acute hepatitis can result from a single large exposure to one of the hepatotoxic agents. These substances may be ingested, inhaled as toxic fumes, or absorbed through the skin. In general, once significant exposure has occurred, a 3-phase clinical syndrome of acute hepatic injury occurs.
      • During phase 1, patients develop gastrointestinal symptoms such as nausea, vomiting, diarrhea, and abdominal pain. They also may exhibit delirium, seizures, or coma representing associated central nervous system toxicity.
      • Between 24-48 hours after exposure, patients enter phase 2; they often experience resolution of their symptoms.
      • Phase 3 occurs 48-72 hours after exposure with the development of fulminant hepatic failure, often accompanied by renal failure. Some of these patients may deteriorate to the point that they face death or require emergent liver transplantation.
  • Autoimmune hepatitis
    • Autoimmune hepatitis is a progressive inflammatory disease of the liver that occurs more commonly in young women and girls. The etiology is not known, but indications are that a certain environmental trigger incites an autoimmune response directed against the liver. These triggers might be viruses, chemicals, or other unknown agents.
    • The resulting chronic hepatitis eventually leads to fibrosis and cirrhosis. Autoimmune hepatitis also is associated with progression to primary hepatocellular carcinoma but not with the same frequency as viral hepatitis.
    • As with other forms of hepatitis, the clinical presentation of autoimmune hepatitis may vary.
    • Patients may be asymptomatic, or they may present with insidious onset of constitutional symptoms and jaundice. Occasionally, patients may develop acute onset of symptoms, significant jaundice, and elevated transaminases mimicking severe viral hepatitis.
    • Patients with autoimmune hepatitis have circulating autoantibodies in their serum and often have elevated serum globulins, gamma globulins in particular.
    • Other autoimmune diseases that may affect these patients include Graves disease, idiopathic thrombocytopenic purpura, pulmonary fibrosis, vitiligo, ulcerative colitis, glomerulonephritis, insulin-dependent diabetes mellitus, and myasthenia gravis.

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Keywords

viral hepatitis, viral hepatitis treatment, viral hepatitis causes, viral hepatitis symptoms, hepatitis A, HAV, epidemic hepatitis, infectious hepatitis, short-incubation hepatitis, virus A hepatitis, viral hepatitis type A, hepatitis B, HBV, viral hepatitis type B, long-incubation hepatitis, serum hepatitis, transfusion hepatitis, virus B hepatitis, hepatitis C, HCV, viral hepatitis type C, hepatitis D, viral hepatitis type D, delta hepatitis, hepatitis E, viral hepatitis type E, liver disease, liver, inflammation of the liver, hepatic failure, hepatic disease, infectious hepatitis, noninfectious hepatitis, drug-induced hepatitis, autoimmune hepatitis, liver transplantation, liver transplant

Contributor Information and Disclosures

Author

Adrienne M Buggs, MD, FACEP, FAAEM,, Medical Director, Drug Enforcement Administration Training Academy Health Unit; Consulting Staff, Department of Emergency Medicine, Dewitt Army Hospital
Adrienne M Buggs, MD, FACEP, FAAEM, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph K Lim, MD, Assistant Professor of Medicine, Director, Yale Viral Hepatitis Program, Section of Digestive Diseases, Yale University School of Medicine
Joseph K Lim, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eugene Hardin, MD, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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