eMedicine Specialties > Emergency Medicine > Gastrointestinal
Viral Hepatitis: Follow-up
Updated: Jul 7, 2009
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.
More on Viral Hepatitis |
| Overview: Viral Hepatitis |
| Differential Diagnoses & Workup: Viral Hepatitis |
| Treatment & Medication: Viral Hepatitis |
Follow-up: Viral Hepatitis |
| References |
| « Previous Page |
References
Wasley A, Grytdal S, Gallagher K. Surveillance for acute viral hepatitis--United States, 2006. MMWR Surveill Summ. Mar 21 2008;57(2):1-24. [Medline]. [Full Text].
Previsani N, Lavanchy D. World Health Organization. Hepatitis B (WHO/CDS/CSR/LYO/2002.2). 2002;[Full Text].
Previsani N, Lavanchy D. World Health Organization. Hepatitis A (WHO/CDS/CSR/EDC/2000.7). 2000;[Full Text].
Previsani N, Lavanchy D. World Health Organization. Hepatitis C (WHO/CDS/CSR/LYO/2003.). 2002;[Full Text].
Krawitt EL. Autoimmune hepatitis: classification, heterogeneity, and treatment. Am J Med. Jan 17 1994;96(1A):23S-26S. [Medline].
Adhami T, Levinthal G. Hepatitis D. The Cleveland Clinic Disease Management Project. May 29, 2002.
Previsani N, Lavanchy D. World Health Organization. Hepatitis D. (WHO/CDS/CSR/NCS/2001.1). 2001;[Full Text].
Previsani N, Lavanchy D. World Health Organization. Hepatitis E. (WHO/CDS/CSR/EDC/2001.12.). 2001;[Full Text].
Adhami T, Levinthal G. Hepatitis E and Hepatitis G/GBV-C. The Cleveland Clinic Disease Management Project. May 29, 2002.
[Guideline] Update: Prevention of hepatitis A after exposure to hepatitis A virus and in international travelers. Updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep. Oct 19 2007;56(41):1080-4. [Medline]. [Full Text].
[Guideline] Centers for Disease Control and Prevention. Viral hepatitis. Hepatitis B vaccination. June 2007;[Full Text].
Alter MJ, Gallagher M, Morris TT, et al. Acute non-A-E hepatitis in the United States and the role of hepatitis G virus infection. Sentinel Counties Viral Hepatitis Study Team. N Engl J Med. Mar 13 1997;336(11):741-6. [Medline].
Alter MJ, Mast EE. The epidemiology of viral hepatitis in the United States. Gastroenterol Clin North Am. Sep 1994;23(3):437-55. [Medline].
Baffis V, Shrier I, Sherker AH, Szilagyi A. Use of interferon for prevention of hepatocellular carcinoma in cirrhotic patients with hepatitis B or hepatitis C virus infection. Ann Intern Med. Nov 2 1999;131(9):696-701. [Medline].
Balfour HH Jr. Antiviral drugs. N Engl J Med. Apr 22 1999;340(16):1255-68. [Medline].
Barash C, Conn MI, DiMarino AJ Jr, Marzano J, Allen ML. Serologic hepatitis B immunity in vaccinated health care workers. Arch Intern Med. Jul 12 1999;159(13):1481-3. [Medline].
Bondesson JD, Saperston AR. Hepatitis. Emerg Med Clin North Am. Nov 1996;14(4):695-718. [Medline].
Boni C, Bertoletti A, Penna A, et al. Lamivudine treatment can restore T cell responsiveness in chronic hepatitis B. J Clin Invest. Sep 1 1998;102(5):968-75. [Medline].
Buti M, Esteban R. Entecavir, FTC, L-FMAU, LdT and others. J Hepatol. 2003;39 Suppl 1:S139-42. [Medline].
Clay KD, Hanson JS, Pope SD, Rissmiller RW, Purdum PP 3rd, Banks PM. Brief communication: severe hepatotoxicity of telithromycin: three case reports and literature review. Ann Intern Med. Mar 21 2006;144(6):415-20. [Medline].
de Groen PC. Hepatitis E in the United States: a case of "hog fever"?. Mayo Clin Proc. Dec 1997;72(12):1197-8. [Medline].
Dinsmoor MJ. Hepatitis in the obstetric patient. Infect Dis Clin North Am. Mar 1997;11(1):77-91. [Medline].
Dusheiko G, Barnes E, Webster G, Whalley S. The science, economics, and effectiveness of combination therapy for hepatitis C. Gut. Aug 2000;47(2):159-61. [Medline].
Dykhuizen RS, Brunt PW, Atkinson P, Simpson JG, Smith CC. Ecstasy induced hepatitis mimicking viral hepatitis. Gut. Jun 1995;36(6):939-41. [Medline].
Fishman LN, Jonas MM, Lavine JE. Update on viral hepatitis in children. Pediatr Clin North Am. Feb 1996;43(1):57-74. [Medline].
Furbee RB, Barlotta KS, Allen MK, Holstege CP. Hepatotoxicity associated with herbal products. Clin Lab Med. Mar 2006;26(1):227-41, x. [Medline].
Galan MV, Potts JA, Silverman AL, Gordon SC. The burden of acute nonfulminant drug-induced hepatitis in a United States tertiary referral center [corrected]. J Clin Gastroenterol. Jan 2005;39(1):64-7. [Medline].
Gross JB Jr. Clinician's guide to hepatitis C. Mayo Clin Proc. Apr 1998;73(4):355-60; quiz 361. [Medline].
Guntupalli SR, Steingrub J. Hepatic disease and pregnancy: an overview of diagnosis and management. Crit Care Med. Oct 2005;33(10 Suppl):S332-9. [Medline].
Hirschman SZ. Current therapeutic approaches to viral hepatitis. Clin Infect Dis. Apr 1995;20(4):741-3; quiz 746. [Medline].
Hoofnagle JH, di Bisceglie AM. The treatment of chronic viral hepatitis. N Engl J Med. Jan 30 1997;336(5):347-56. [Medline].
Hugle T, Cerny A. Current therapy and new molecular approaches to antiviral treatment and prevention of hepatitis C. Rev Med Virol. Nov-Dec 2003;13(6):361-71. [Medline].
Kane MA. Hepatitis viruses and the neonate. Clin Perinatol. Mar 1997;24(1):181-91. [Medline].
Kanel GC, Cassidy W, Shuster L, Reynolds TB. Cocaine-induced liver cell injury: comparison of morphological features in man and in experimental models. Hepatology. Apr 1990;11(4):646-51. [Medline].
Koff RS. Hepatitis A. Lancet. May 30 1998;351(9116):1643-9. [Medline].
Krawitt EL. Autoimmune hepatitis. N Engl J Med. Apr 4 1996;334(14):897-903. [Medline].
Kwo PY, Schlauder GG, Carpenter HA, et al. Acute hepatitis E by a new isolate acquired in the United States. Mayo Clin Proc. Dec 1997;72(12):1133-6. [Medline].
Lai CL, Ratziu V, Yuen MF, Poynard T. Viral hepatitis B. Lancet. Dec 20 2003;362(9401):2089-94. [Medline].
Lee WM. Hepatitis B virus infection. N Engl J Med. Dec 11 1997;337(24):1733-45. [Medline].
Lemon SM, Thomas DL. Vaccines to prevent viral hepatitis. N Engl J Med. Jan 16 1997;336(3):196-204. [Medline].
Levy MJ, Herrera JL, DiPalma JA. Immune globulin and vaccine therapy to prevent hepatitis A infection. Am J Med. Nov 1998;105(5):416-23. [Medline].
Liang TJ, Rehermann B, Seeff LB, Hoofnagle JH. Pathogenesis, natural history, treatment, and prevention of hepatitis C. Ann Intern Med. Feb 15 2000;132(4):296-305. [Medline].
Lutwick LI. Postexposure prophylaxis. Infect Dis Clin North Am. Dec 1996;10(4):899-915. [Medline].
Mieli-Vergani G, Vergani D. Autoimmune hepatitis. Arch Dis Child. Jan 1996;74(1):2-5. [Medline].
Poordad FF, Tran T, Martin P. Developments in hepatitis C therapy during 2000-2002. Expert Opin Emerg Drugs. May 2003;8(1):9-25. [Medline].
Poynard T, Yuen MF, Ratziu V, Lai CL. Viral hepatitis C. Lancet. Dec 20 2003;362(9401):2095-100. [Medline].
Public Health. Hepatitis A. CMAJ. Feb 15 1997;156(4):545-6. [Medline].
Purcell RH. The discovery of the hepatitis viruses. Gastroenterology. Apr 1993;104(4):955-63. [Medline].
Sagliocca L, Amoroso P, Stroffolini T, et al. Efficacy of hepatitis A vaccine in prevention of secondary hepatitis A infection: a randomised trial. Lancet. Apr 3 1999;353(9159):1136-9. [Medline].
Sjogren MH. Serologic diagnosis of viral hepatitis. Gastroenterol Clin North Am. Sep 1994;23(3):457-77. [Medline].
Tepper MI, Gully PR. Viral hepatitis: know your D, E, F and Gs. CMAJ. Jun 15 1997;156(12):1735-8. [Medline].
[Guideline] The Centers for Disease Control and Prevention. From the Centers for Disease Control and Prevention. Update: recommendations to prevent hepatitis B virus transmission--United States. JAMA. Mar 3 1999;281(9):790. [Medline].
Thomas DL, Astemborski J, Rai RM, et al. The natural history of hepatitis C virus infection: host, viral, and environmental factors. JAMA. Jul 26 2000;284(4):450-6. [Medline].
Zimmerman HJ, Lewis JH. Chemical- and toxin-induced hepatotoxicity. Gastroenterol Clin North Am. Dec 1995;24(4):1027-45. [Medline].
Further Reading
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
Follow-up: Viral Hepatitis