## Diagnosis: Acute Hepatitis A ### Clinical Presentation The patient presents with the classic triad of acute viral hepatitis: - **Prodromal phase**: Jaundice, dark urine, abdominal pain - **Timeline**: Symptom onset 10 days after exposure (incubation period 15–50 days, typically 28–30 days for HAV) - **Epidemiology**: Rural setting with contaminated water exposure — HAV is fecal-oral transmitted ### Serological Confirmation | Marker | Result | Interpretation | |--------|--------|----------------| | Anti-HAV IgM | **Positive** | Acute infection (diagnostic) | | Anti-HAV IgG | Negative | No prior immunity | | HBsAg | Negative | No HBV co-infection | | Anti-HCV | Negative | No HCV co-infection | **Key Point:** Anti-HAV IgM is the gold standard for diagnosing acute hepatitis A and appears early in the illness, during the symptomatic phase. ### Laboratory Pattern - **Marked transaminitis**: ALT > AST (2840 IU/L) — typical of acute viral hepatitis - **Cholestasis**: Elevated ALP and direct hyperbilirubinemia - **Preserved synthetic function**: Albumin 3.8 g/dL, PT-INR 1.2 (no fulminant failure) - **Pattern**: Hepatocellular injury predominates (ALT >> ALP) ### Clinical Course **High-Yield:** Hepatitis A is typically **self-limited** with complete recovery in 4–12 weeks. No chronic carrier state develops. Fulminant hepatic failure occurs in <1% of cases (more common in older patients and those with underlying liver disease). **Clinical Pearl:** The presence of normal PT-INR and preserved albumin argues against fulminant hepatic failure, making this uncomplicated acute HAV infection. ### Management Principles 1. Supportive care (hydration, rest) 2. Monitor for fulminant hepatic failure (PT-INR, bilirubin trend) 3. Avoid hepatotoxic drugs 4. Contacts: HAV vaccine or immunoglobulin prophylaxis within 2 weeks of exposure [cite:Harrison 21e Ch 304]
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