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Hepatitis

From Surgopaedia

Acute hepatitis

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    • Aetiology
      • Viral hepatitis (see below)
      • Drugs - including paracetamol overdose (can occur with small amounts in alcoholics)
      • Acute alcoholic hepatitis
      • Gallstones
      • Wilson's disease, especially in childhood
      • In pregnancy - acute viral hepatitis is most common, but consider acute fatty liver
    • Symptoms:
      • Nausea +/- vomiting
      • RUQ pain
      • Weakness/fatigue
      • Fever
      • Pruritis
      • Jaundice
    • Examination
      • Tender hepatomegaly often seen
      • Check for complications such as encephalopathy
    • Investigation
      • Transaminase usually >5x ULN
      • Moderate ALP elevations can occur
      • USS - look at liver and spleen and exclude biliary disease
    • Management
      • Viral hepatitis - supportive, ensure they don't develop fulminant liver failure, or develop chronic disease
      • Withdraw offending drugs
      • Alcoholic hepatitis - supportive, nutritional supplementation, thiamine, corticosteroids if encephalopathy
      • Acute autoimmune hepatitis - corticosteroids (e.g. prednisolone 30-60mg daily then taper)


Viral hepatitis

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    • Most relevant to surgeons in the setting of patients with chronic hepatitis needing liver surgery, and the influence on functional liver remnant

Epidemiology

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      • Most common cause of liver disease worldwide (>5 million people)

Aetiology/pathophysiology

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      • HAV
        • Faecal-oral
        • Humans are the only hosts
        • Acute inflammation of the liver with no known chronic sequelae
        • Fulminant hepatitis develops in 1-5% of cases, with mortality <1%
      • HBV
        • Only viral hepatitis with a DNA genome (others RNA)
        • 70% of patients with acute HBV have subclinical or an-icteric infection; the other 30% have icteric hepatitis
        • Incubation 1-4 months
        • Prodromal serum sickness-like infection, followed by constitutional symptoms lasting for 10 days, then jaundice
        • Clinical symptoms usually disappear in 3/12
        • Fulminant hepatic failure in 0.1-0.5%, and 80% mortality rate unless liver transplantation is performed
        • Risk of chronic HBV is related to immunocompetence and age
          • Immunocompetent adults <5%
          • Children 30%
          • Infants 90%
        • Chronic HBV has different phases
          • HbeAg-positive chronic infection
          • HBeAg-positive chronic hepatitis B - elevated ALT, suggesting liver damage
          • HBeAg-negative chronic HBV infection
          • HBeAg-negative chronic hepatitis B
        • Complications of chronic HBV
          • Cirrhosis
          • HCC
          • Hepatic failure
          • Death
        • Extra-hepatic manifestations of chronic HBV:
          • Polyarteritis nodosa
          • Glomerulonephritis
          • Essential mixed cryoglobulinaemia
          • Papular acrodermatitis
      • HCV
        • IVDU
        • Commonly appears 20-39yo
        • Single-stranded RNA genome which replicates in the hepatocyte cytoplasm
        • Acute HCV - mild elevation of hepatocellular enzyme levels - 5-12 weeks post-infection, with mild symptoms if any. Jaundice in <20%.
        • Fulminant hepatic failure is extremely uncommon
        • Chronic HCV develops in two thirds of patients - mostly asymptomatic, but at risk of cirrhosis (2-20% over 20-30 years) and subsequently HCC (1-4% per year)
          • Progresses faster in men, older age at infection, immunosuppression, co-infection with HBV, moderate alcohol intake, and obesity
      • HDV
        • Delta virus
        • Requires HBV co-infection
      • HEV - unique enteral form
        • Cholestatic LFTs in most
        • Incubation 2-9 weeks
        • Jaundice in >90%
        • Usually self-limiting
      • HGV
        • Still being defined
        • Similarities to HCV
        • No definitive association with clinical hepatitis

Treatment

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    • HAV or HEV: supportive, correct dehydration, provide adequate calories
    • HBV
      • Chronic active disease - interferon-alpha and lamivudine, and other nucleoside analogues, can induce viral suppression but not cure. Leads to regression of cirrhosis. Decision to treat depends on serum HBV DNA levels, serum ALT levels, and severity of liver disease. Cirrhosis with or without decompensation + detectable serum DNA is an indication for treatment.
    • HCV
      • Direct-acting antivirals are effective at cure in >90% of patients