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Emergency And Acute Medicine – Hepatitis
Basics And Description
Hepatitis refers to inflammation of the liver caused by infectious, toxic, metabolic, or autoimmune processes. Disease progression may range from transient hepatocellular injury to fibrosis, cirrhosis, and liver failure. Infectious causes, particularly viral hepatitis, account for the majority of cases encountered in emergency and acute care settings.
Etiology
No specific cause is identified in approximately 5–10% of acute and chronic hepatitis cases and up to 50% of fulminant hepatic failure.
Hepatitis A is transmitted via the fecal–oral route with an incubation period of 2–7 weeks. It does not cause chronic disease, though up to 10% of patients experience a relapsing course. Fulminant hepatic failure occurs in about 0.1%.
Hepatitis B is transmitted through percutaneous or mucosal exposure to body fluids and perinatally, with an incubation period of 8–22 weeks. Most infections are subclinical. Risk of chronic infection depends on age and immune status and carries long-term risks of cirrhosis and hepatocellular carcinoma.
Hepatitis C is primarily bloodborne, with sexual and perinatal transmission occurring less commonly. Incubation is 6–10 weeks. Fulminant hepatic failure is rare, but approximately 80% progress to chronic disease with risk of cirrhosis and hepatocellular carcinoma.
Hepatitis D occurs only in the presence of hepatitis B, either as coinfection or superinfection, and is associated with a higher risk of cirrhosis.
Hepatitis E is the most common cause of acute hepatitis worldwide, transmitted fecal–orally, often via contaminated water. Fulminant hepatic failure occurs in up to 10% and is particularly severe in pregnancy.
Alcoholic hepatitis results from chronic heavy alcohol use and may progress to cirrhosis. Severity can be estimated using the Maddrey discriminant function.
Other causes include abscess-related hepatitis, secondary viral infections such as CMV or EBV, medication- or toxin-induced injury, and autoimmune hepatitis.
In children, hepatitis A predominates, while perinatal hepatitis B commonly progresses to chronic disease. In pregnancy, hepatitis E carries high mortality, and pregnancy-specific liver diseases such as acute fatty liver of pregnancy and HELLP syndrome must be considered.
Diagnosis – Signs And Symptoms
Many patients are asymptomatic. The preicteric phase may mimic viral gastroenteritis with fever, malaise, nausea, vomiting, anorexia, and arthralgia. The icteric phase includes jaundice, dark urine, light stools, pruritus, rash, and right upper quadrant pain. Fulminant hepatic failure presents with coagulopathy, encephalopathy, cerebral edema, bleeding, and altered mental status.
Physical Examination
Findings vary by disease phase. Early disease may show fever, dehydration, or arthritis. Icteric findings include jaundice of skin and sclerae, tender hepatomegaly, rash, and dehydration. Severe disease may demonstrate bruising, asterixis, and disorientation.
Essential Workup
A detailed history focusing on travel, exposures, alcohol use, medications, and risk factors is critical. Viral serologies are central to diagnosis of infectious causes.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, metabolic panel, liver function tests, coagulation studies, albumin, and glucose. Transaminase elevation reflects hepatocellular injury but does not correlate reliably with severity. Markedly elevated alkaline phosphatase suggests cholestatic disease. Prolonged INR and low albumin indicate impaired synthetic function. Ammonia levels are useful in altered mental status.
Viral serologies define etiology, including HAV IgM, HBV surface and core antibodies, HCV antibody and RNA, HDV testing when indicated, and HEV IgM. Additional tests include α-fetoprotein in chronic viral hepatitis, Monospot testing for EBV, and urinalysis for bilirubin.
Imaging includes right upper quadrant ultrasound to assess for biliary obstruction and head CT when hepatic encephalopathy is suspected.
Differential Diagnosis
Consider nonalcoholic fatty liver disease, biliary disease, ischemic hepatitis, congestive heart failure, metabolic and genetic disorders, liver abscess, heat stroke, Wilson disease, Budd–Chiari syndrome, and pregnancy-related liver disease.
Initial Stabilization And Therapy
Airway, breathing, and circulation are priorities in fulminant hepatic failure or severe encephalopathy. Judicious intravenous fluid resuscitation is required.
Emergency Department Treatment And Procedures
Management is largely supportive. Correct hypovolemia and electrolyte disturbances, treat nausea and vomiting, and avoid hepatotoxic medications and alcohol. Use medications with minimal hepatic metabolism when sedation or analgesia is required. Correct coagulopathy only in the presence of active bleeding. Administer N-acetylcysteine for acetaminophen toxicity and consider its use in fulminant hepatic failure. Steroids may benefit severe alcoholic hepatitis. Manage pruritus with bile acid sequestrants. Perform paracentesis for tense ascites causing respiratory compromise. Provide postexposure prophylaxis for hepatitis A and B when indicated.
Medications
Commonly used agents include ondansetron or metoclopramide for nausea, cholestyramine or ursodeoxycholic acid for pruritus, N-acetylcysteine, prednisone for select alcoholic hepatitis cases, vitamin K for coagulopathy, and thiamine in malnourished patients.
Follow-Up And Disposition
Admit patients with intractable vomiting, dehydration, electrolyte abnormalities, pregnancy, immunocompromise, suspected toxic hepatitis, advanced age, or evidence of significant liver dysfunction. Fulminant hepatic failure requires ICU care and early transfer to a transplant center. Patients with mild disease and good oral tolerance may be discharged with close follow-up.
Follow-Up Recommendations
Arrange hepatology or gastroenterology follow-up for definitive diagnosis and management. Counsel on strict hygiene, avoidance of alcohol and acetaminophen, vaccination when appropriate, and limitation of strenuous activity.
Clinical Insights And Common Errors
Acute hepatitis is frequently misdiagnosed as a nonspecific viral illness. Emergency management is primarily supportive. Early recognition of fulminant hepatic failure and prompt transfer to a transplant-capable center are critical. Maintain high suspicion for pregnancy-related liver disease in pregnant patients with compatible symptoms.
Basics And Description
Hepatitis refers to inflammation of the liver caused by infectious, toxic, metabolic, or autoimmune processes. Disease progression may range from transient hepatocellular injury to fibrosis, cirrhosis, and liver failure. Infectious causes, particularly viral hepatitis, account for the majority of cases encountered in emergency and acute care settings.
Etiology
No specific cause is identified in approximately 5–10% of acute and chronic hepatitis cases and up to 50% of fulminant hepatic failure.
Hepatitis A is transmitted via the fecal–oral route with an incubation period of 2–7 weeks. It does not cause chronic disease, though up to 10% of patients experience a relapsing course. Fulminant hepatic failure occurs in about 0.1%.
Hepatitis B is transmitted through percutaneous or mucosal exposure to body fluids and perinatally, with an incubation period of 8–22 weeks. Most infections are subclinical. Risk of chronic infection depends on age and immune status and carries long-term risks of cirrhosis and hepatocellular carcinoma.
Hepatitis C is primarily bloodborne, with sexual and perinatal transmission occurring less commonly. Incubation is 6–10 weeks. Fulminant hepatic failure is rare, but approximately 80% progress to chronic disease with risk of cirrhosis and hepatocellular carcinoma.
Hepatitis D occurs only in the presence of hepatitis B, either as coinfection or superinfection, and is associated with a higher risk of cirrhosis.
Hepatitis E is the most common cause of acute hepatitis worldwide, transmitted fecal–orally, often via contaminated water. Fulminant hepatic failure occurs in up to 10% and is particularly severe in pregnancy.
Alcoholic hepatitis results from chronic heavy alcohol use and may progress to cirrhosis. Severity can be estimated using the Maddrey discriminant function.
Other causes include abscess-related hepatitis, secondary viral infections such as CMV or EBV, medication- or toxin-induced injury, and autoimmune hepatitis.
In children, hepatitis A predominates, while perinatal hepatitis B commonly progresses to chronic disease. In pregnancy, hepatitis E carries high mortality, and pregnancy-specific liver diseases such as acute fatty liver of pregnancy and HELLP syndrome must be considered.
Diagnosis – Signs And Symptoms
Many patients are asymptomatic. The preicteric phase may mimic viral gastroenteritis with fever, malaise, nausea, vomiting, anorexia, and arthralgia. The icteric phase includes jaundice, dark urine, light stools, pruritus, rash, and right upper quadrant pain. Fulminant hepatic failure presents with coagulopathy, encephalopathy, cerebral edema, bleeding, and altered mental status.
Physical Examination
Findings vary by disease phase. Early disease may show fever, dehydration, or arthritis. Icteric findings include jaundice of skin and sclerae, tender hepatomegaly, rash, and dehydration. Severe disease may demonstrate bruising, asterixis, and disorientation.
Essential Workup
A detailed history focusing on travel, exposures, alcohol use, medications, and risk factors is critical. Viral serologies are central to diagnosis of infectious causes.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, metabolic panel, liver function tests, coagulation studies, albumin, and glucose. Transaminase elevation reflects hepatocellular injury but does not correlate reliably with severity. Markedly elevated alkaline phosphatase suggests cholestatic disease. Prolonged INR and low albumin indicate impaired synthetic function. Ammonia levels are useful in altered mental status.
Viral serologies define etiology, including HAV IgM, HBV surface and core antibodies, HCV antibody and RNA, HDV testing when indicated, and HEV IgM. Additional tests include α-fetoprotein in chronic viral hepatitis, Monospot testing for EBV, and urinalysis for bilirubin.
Imaging includes right upper quadrant ultrasound to assess for biliary obstruction and head CT when hepatic encephalopathy is suspected.
Differential Diagnosis
Consider nonalcoholic fatty liver disease, biliary disease, ischemic hepatitis, congestive heart failure, metabolic and genetic disorders, liver abscess, heat stroke, Wilson disease, Budd–Chiari syndrome, and pregnancy-related liver disease.
Initial Stabilization And Therapy
Airway, breathing, and circulation are priorities in fulminant hepatic failure or severe encephalopathy. Judicious intravenous fluid resuscitation is required.
Emergency Department Treatment And Procedures
Management is largely supportive. Correct hypovolemia and electrolyte disturbances, treat nausea and vomiting, and avoid hepatotoxic medications and alcohol. Use medications with minimal hepatic metabolism when sedation or analgesia is required. Correct coagulopathy only in the presence of active bleeding. Administer N-acetylcysteine for acetaminophen toxicity and consider its use in fulminant hepatic failure. Steroids may benefit severe alcoholic hepatitis. Manage pruritus with bile acid sequestrants. Perform paracentesis for tense ascites causing respiratory compromise. Provide postexposure prophylaxis for hepatitis A and B when indicated.
Medications
Commonly used agents include ondansetron or metoclopramide for nausea, cholestyramine or ursodeoxycholic acid for pruritus, N-acetylcysteine, prednisone for select alcoholic hepatitis cases, vitamin K for coagulopathy, and thiamine in malnourished patients.
Follow-Up And Disposition
Admit patients with intractable vomiting, dehydration, electrolyte abnormalities, pregnancy, immunocompromise, suspected toxic hepatitis, advanced age, or evidence of significant liver dysfunction. Fulminant hepatic failure requires ICU care and early transfer to a transplant center. Patients with mild disease and good oral tolerance may be discharged with close follow-up.
Follow-Up Recommendations
Arrange hepatology or gastroenterology follow-up for definitive diagnosis and management. Counsel on strict hygiene, avoidance of alcohol and acetaminophen, vaccination when appropriate, and limitation of strenuous activity.
Clinical Insights And Common Errors
Acute hepatitis is frequently misdiagnosed as a nonspecific viral illness. Emergency management is primarily supportive. Early recognition of fulminant hepatic failure and prompt transfer to a transplant-capable center are critical. Maintain high suspicion for pregnancy-related liver disease in pregnant patients with compatible symptoms.
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