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Viral Hepatitis Clinical Presentation

  • Author: Adrienne M Buggs, MD, FACEP, FAAEM; Chief Editor: Steven C Dronen, MD, FAAEM  more...
 
Updated: Dec 16, 2014
 

History

The clinical presentation of infectious hepatitis varies with the individual, as well as with the specific causative virus. Some patients may be entirely asymptomatic or only mildly symptomatic at presentation. Others may present with rapid onset of fulminant hepatic failure (FHF). The classic presentation of infectious hepatitis involves 4 phases, as follows:

  • Phase 1 (viral replication phase) – 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, and 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 (GI) symptoms and malaise, patients become icteric and may develop right upper quadrant pain with hepatomegaly
  • Phase 4 (convalescent phase) – Symptoms and icterus resolve, and liver enzymes return to normal

Hepatitis A

The incubation period of hepatitis A virus (HAV) is 2-7 weeks (average, 28 days). Clinical symptoms then develop, often with a presentation similar to that of gastroenteritis or a viral respiratory infection. The most common signs and symptoms include fatigue, nausea, vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, and rash.

HAV infection usually occurs as a mild self-limited disease and confers lifelong immunity to the virus. Chronic HAV infection does not occur.

Hepatitis B

The incubation period for hepatitis B virus (HBV) is 30-180 days (average, approximately 75 days). Patients then enter the prodromal or preicteric phase, characterized by the 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. About 15% 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, the clinical course may be highly variable. Whereas some patients experience fairly rapid improvements in their symptoms, others go on to experience prolonged disease with slow resolution. Still others may have symptoms that periodically improve, only to worsen later (relapsing hepatitis). Finally, there is an unfortunate subset of patients in whom the disease rapidly progresses to FHF; this may occur over days to weeks.

Hepatitis C

The incubation period for hepatitis C virus (HCV) is 15-150 days, with symptoms developing anywhere from 5-12 weeks after exposure. During acute HCV infection, symptoms may appear similar to those of HBV infection. In up to 80% of cases, however, patients are asymptomatic and do not develop icterus.[1, 16]

Hepatitis D

The incubation period of hepatitis D virus (HDV) is approximately 35 days. Patients simultaneously infected with HBV and HDV often have an acute, self-limited infection.[19, 27] Fewer than 5% of these patients develop chronic HDV infection.

Chronic HBV carriers who become superinfected with HDV tend to have a more severe acute hepatitis; 80% of these patients go on to develop chronic HDV infection. Chronic infection with HBV and HDV may lead to fulminant acute hepatitis and severe chronic active hepatitis with progression to cirrhosis.[19, 27] Over the long term, as many as 70-80% of these patients have evidence of chronic liver disease with cirrhosis, compared with only 15-30% of patients with chronic HBV alone.

Hepatitis E

The incubation period of hepatitis E virus (HEV) is 2-9 weeks (average, 45 days). HEV usually causes an acute self-limited disease similar to HASV infection. Fulminant disease does occur in about 10% of cases. In women who are pregnant, HEV infection has a case-fatality rate of 15-20%.[21] No reports exist of chronic infection with HEV.[21]

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Physical Examination

Physical findings in patients with hepatitis vary with the type of hepatitis and the 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 suspect an abscess or tumor.

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Complications

In general, complications of viral hepatitis may include the following:

  • Acute or subacute hepatic necrosis
  • Chronic active hepatitis
  • Chronic hepatitis
  • Hepatic failure
  • Hepatocellular carcinoma (HCC) in patients with HBV or HCV infection

Hepatitis B

One of the major complications of hepatitis B is the development of chronic infection. An estimated 350 million people worldwide are chronically infected with HBV.[2] In the United States, 1.25 million people are estimated to have chronic HBV infection.[1] Patients with such infection are at risk for the subsequent development of chronic active hepatitis, cirrhosis of the liver, and eventual HCC. Each year, approximately 1 million deaths occur worldwide as a result of chronic HBV infection.[2]

Patients infected at an early age are at greatest risk for chronic HBV infection: Whereas 90% of those infected at birth develop chronic HBV infection, 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 HBV infection are at significantly higher risk for HCC. In fact, HCC is the leading cause of cancer-related deaths in areas where HBV is endemic. Globally, HBV 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. HCC develops an average of 25-30 years after initial infection.

Another major complication of HBV infection is development of FHF. In approximately 0.5-1% of HBV-infected patients, the disease progresses to FHF, with coagulopathy, encephalopathy, and cerebral edema. The case-fatality rate for these patients approaches 80%.[2]

Hepatitis C

Acute infection with HCV may rarely cause FHF.[16] Approximately 70-90% of patients with hepatitis C 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.[16]

Cirrhosis related to chronic HCV infection is also strongly linked to the development of HCC, 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.[16] In the United States, cirrhosis associated with chronic hepatitis C is a leading indication for liver transplant.[16]

Extrahepatic complications

Patients with chronic hepatitis C are also at risk for extrahepatic complications. In essential mixed cryoglobulinemia, HCV may form immune complexes with anti-HCV immunoglobulin G (IgG) and with rheumatoid factor (RF). The deposition of immune complexes may cause small-vessel damage. Complications of cryoglobulinemia include rash, vasculitis, and glomerulonephritis.

Other extrahepatic complications of HCV infection include focal lymphocytic sialadenitis, autoimmune thyroiditis, porphyria cutanea tarda, lichen planus, and Mooren corneal ulcer. Some cases of non-Hodgkin lymphoma can be attributed to HCV infection.

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Contributor Information and Disclosures
Author

Adrienne M Buggs, MD, FACEP, FAAEM Medical Director, Drug Enforcement Administration Training Academy Health Unit

Adrienne M Buggs, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Eugene Hardin, 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.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Joseph K Lim, MD Associate 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.

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.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rajeev Vasudeva, MD, FACG Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association

Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting

David C Wolf, MD, FACP, FACG, AGAF Medical Director of Liver Transplantation, Westchester Medical Center; Professor of Clinical Medicine, Division of Gastroenterology and Hepatobiliary Diseases, Department of Medicine, New York Medical College

David C Wolf, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, and American Gastroenterological Association

Disclosure: Nothing to disclose.

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Hepatitis A virus as viewed through electron microscopy.
Liver biopsy specimen showing ground-glass appearance of hepatocytes in patient with hepatitis B.
Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in patient with hepatitis B.
Liver biopsy with trichrome stain showing stage 3 fibrosis in patient with hepatitis B.
Hepatic carcinoma, primary. Large multifocal hepatocellular carcinoma in 80-year-old man without cirrhosis.
Triple-phase CT scan of liver cancer, revealing classic findings of enhancement during arterial phase and delayed hypointensity during portal venous phase.
Table 1. Diagnostic Tests for Hepatitis B
Test CHB HBeAg Positive CHB HBeAg Negative Inactive Carrier
HBsAg + + +
Anti-HBs - - -
HBeAg + - -
Anti-HBe - + +
Anti-HBc + + +
IgM anti-HBc - - -
HBV DNA >2 × 104 IU/mL*



(>105 copies/mL)



>2 × 103 IU/mL



(>104 copies/mL)



< 2 × 103 IU/mL



(< 104 copies/mL)



ALT level Elevated Elevated Normal
ALT = alanine aminotransferase; anti-HBc = antibody to hepatitis B core antigen; anti-HBe = antibody to HBeAg; anti-HBs = antibody to HBsAg; CHB = chronic hepatitis B; HBV = hepatitis B virus; HBeAg = hepatitis B e antigen; HBsAg = hepatitis B surface antigen; IgM = immunoglobulin M.



*Increasingly, experts in the field use IU/mL rather than copies/mL.



Table 2. Histologic Grading for Hepatitis C–Induced Liver Disease
Grade Portal Inflammation Interface Hepatitis Lobular Necrosis
1 - Minimal Mild Scant None
2 - Mild Mild Mild Scant
3 - Moderate Moderate Moderate Spotty
4 - Severe Marked Marked Confluent
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